I 



I 




4 * < 




A 



TEXT-BOOK 




3 

PATHOLOGY 



/ BY 

ALFRED STENGEL, M. D. 

Professor of Clinical Medicine in the University of Pennsylvania ; Physician to 
the Philadelphia Hospital ; Physician to the Children's 
Hospital, Philadelphia, etc. 



IX 



HflUtb 372 ITilustrattons 



THIRD EDITION, REVISED 



PHILADELPHIA and LONDON 

W. B, SAUNDERS & COMPANY 

1900 



56678 

"'fcU 1.UPIU fttUftffD 

OCT 5 1900 
seccho copy. 

OROttf DIVISION, 

_QCF 13 



Copyright, 1900, by 
W. B. SAUNDERS & COMPANY. 



ELECT ROTYPED BY 
WESTCOTT Sl THOMSON. PHILADA. 



PRESS OF 
W. B. SAUNDERS & COMPANY. 



PREFACE TO THE THIRD EDITION. 



The present edition has been thoroughly revised, with the 
intention of bringing the subject-matter up to date and amplifying 
the sections on Pathologic Physiology. The favorable reception 
of previous editions has convinced the author that his primary 
purpose — viz., to supply a moderate-sized book on Clinical 
Pathology — has found favor with the profession. 

The revision of the sections on Neuro-pathology has been 
kindly undertaken by Dr. Joseph Sailer, to whom the author 
wishes to express his thanks. 

September, 1900. 

5 



PREFACE. 



In writing this book the author has tried to present the sub- 
ject of Pathology in as practical a form as possible, and always 
from the point of view of the clinical pathologist. Considerable 
parts of the book were first prepared and used as the basis of 
demonstrations upon clinical pathology for students of medicine ; 
prominence is therefore given to pathologic physiology, and dis- 
cursiveness and citation of authorities are avoided. 

Except in a few instances, discussion of methods of examina- 
tion has been omitted, because it seemed unwise to increase the 
size of the book Avith matter that is appropriately presented in 
special works on technique. For similar reasons the author has 
decided to exclude the pathology of the skin and of the organs 
of special sense. 

Controversial matter has been avoided as much as possible, 
excepting in certain parts of the sections on General Bacteriology 
and on Neuropathology, in which it seemed proper to discuss 
conflicting theories. 

Full use has been made of works on pathology and of special 
monographs in English as well as in French and German. 

The author is greatly indebted to Dr. Samuel S. Kneass and 
Dr. Alonzo E. Taylor for assistance in the sections on General 
Bacteriology and the Degenerations in Part I., and especially 
to Dr. Joseph Sailer, who prepared almost wholly the sections 
on Neuropathology. Acknowledgment is also due Mr. Thos. 
F. Dagney, of Mr. Saunders' editorial office, for his uniform 
courtesy and assistance in many ways, and Mr. R. W. Greene 
for the preparation of the Index. 



CONTENTS. 



PART I.— GENERAL PATHOLOGY. 



CHAPTER I. 

The Etiology of Disease 18 

Traumatism, 19. — Physical Conditions, 20. — Poisons, 24. — Vegetable 
and Animal Parasites, 31. 

CHAPTER XI. 

Disorders of Nutrition and Metabolism 32 

Food, 32. — Diminished Supply of Food, 33. — Increased Supply of 
Food, 33. — Excessive Tissue-destruction, 34. — Acid-intoxication, 35. — 
Formation of Albumoses, 36. — Alloxin Bases and Uric Acid, 37. — 
Gout, 37. — Glycosuria, 39. — Diabetes, 40. — Fever, 43. 

CHAPTER III. 

Disturbances of the Circulation of the Blood 45 

General Disturbances, 45. — Local Hyperemia, 48. — Local Anemia, 
49. — Hemorrhage, 50. — Embolism, 53. — Infarction, 55. — Thrombosis, 
57. — Edema, 61. 

CHAPTER IV. 

Retrogressive Processes 64 

Atrophy, 64.— The Degenerations, 66.— Cloudy Swelling, 66.— Fatty 
Infiltration, 68. — Fatty Degeneration, 70. — The Albuminoid Degenera- 
tions, 73. — Amyloid Degeneration, 74. — Hyaline Degeneration, 76. — 
Mucoid Degeneration, 79. — Colloid Degeneration, 81. — Glycogenic Infil- 
tration, 82. — Dropsical Infiltration, 83. — Calcification, 84. — Ossification, 
86. — Uratic Infiltration, 86. — Pigmentation, 86. — Necrosis, 91. — Coagu- 
lation-necrosis, 93. — Liquefaction-necrosis, 95. — Caseation, 96. — Fat- 
necrosis. 97. — Hemolysis, 98. — Gangrene, 98. — Cellular Necrosis, 
100. — Post-mortem Alterations, 100. 



CHAPTER V. 

Inflammation and Regeneration 101 

Inflammation, 100. — Regeneration, 116. — Metaplasia, 120. 

9 



10 



CONTENTS. 



CHAPTEK VI. 

PAGE 

Progressive Tissue-changes 120 

Hypertrophy, 120. — Tumors, 121.— Fibroma, 127.— Myxoma, 130.— 
Lipoma, 132. — Xanthoma, 133. — Chondroma, 134. — Osteoma, 137. — 
Lymphangioma, 139. — Hemangioma, 139. — Lymphadenoma, 142. — 
Myeloma, 145. — Sarcoma, 145. — Spindle-celled Sarcoma, 148. — Round- 
celled Sarcoma, 149. — Angiosarcoma, 150. — Cylindroma, 152. — Melano- 
sarcoma, 153. — Giant-celled Sarcoma, 154. — Mixed Tumors, 156. — 
Chloroma, 156. — Psammoma, 156. — Mycosis Fungoi'des, 156. — Endo- 
thelioma, 157. — Glioma, 157. — Neuroma, 161. — Leiomyoma, 161. — 
Rhabdomyoma, 164. — Papilloma, 164. — Adenoma, 166. — Carcinoma, 
170. — Epithelioma, 178. — Glandular Carcinoma, 179. — Colloid Cancer, 
181. — Syncytioma Malignum, 182. — Cysts, 183. — Teratoma, 186. 



CHAPTER VII. 

Bacteria and Diseases due to Bacteria 188 

Classification, 189. — Morphology, 190. — Demonstration, 193. — Biol- 
ogy, 195. — Functions and Products of Bacteria, 199. — The Local Effects 
of Bacteria, 203. — Effects of Toxic Products of Bacteria, 203. — Im- 
munity, 204. 

Diseases due to Bacteria, 210— Suppurative Diseases, 210 — 
Gonorrhea, 215. — Croupous Pneumonia, 216. — Other Forms of Pneu- 
monia, 219. — Rhinoscleroma, 219. — Diphtheria, 220.— Typhoid fever, 
224.— Bacillus Coli Communis, 227.— Cholera, 229 —Tuberculosis, 233. 
— Smegma Bacillus, 243. — Fowl-tuberculosis, 245. — Pseudotuberculosis, 
245. — Leprosy, 245. — Glanders, 249. — Malignant Edema, 251. — An- 
thrax, 252. — Infectious Emphysema, 255. — Tetanus, 256. — Actinomy- 
cosis, 258. — Mycetoma, 261. — Relapsing Fever, 262. — Influenza, 263. — 
Bubonic Plague, 264. — Thrush, 265. — Pharyngomycosis Leptothricia, 
265.— Syphilis. 266.— Soft Chancre, 271.— Yellow Fever, 271.— Measles, 
273.— Scarlet Fever, 273.— Mumps, 273.— Whooping-cough, 273.— 
Typhus Fever, 274. — Rabies, 274. — Proteus Infection, 274. — Hemor- 
rhagic Diseases, 274. — Rheumatism, 275. — Malta Fever, 276. — Beri- 
beri, 277. 



CHAPTER VIII. 

Animal Parasites and Diseases Caused by Them -<~ 

Protozoa, 277.— Amreba Coli, 278.— Other Amebse, 279.— Cerco- 
monas Intestinalis, 279. — Cercomonas Coli Hominis, 279.— Trichomonas 
Intestinalis, 280.— Trichomonas Vaginalis, 280.— Other Forms of 
Trichomonas, 280. — Balantidium Coli, 280.— Megastoma Entericum, 
281.— Hematozoon Malaria?, 282.— Coccidium Oviforme, 285.— Animal 
Parasites and Carcinoma, 287. — Animal Parasites and Molluscum Con- 
tagiosum, 289. — Variola and Vaccinia, 290. — Varicella, 290. — Measles, 
Scarlet Fever, and other Diseases, 290. 



CONTENTS. 



11 



Cestodes, or Tape=worms, 290.— Taenia Solium, 292. — Taenia 
Saginata, 294. — Taenia Nana, 295. — Taenia Elliptica, 296. — Taenia Flavo- 
punctata, 296. — Taenia Madagascariensis, 296. — Other Forms of Taenia, 
296. — Taenia Echinococcus, 297. — Bothriocephalic Latus, 299. — Bothrio- 
cephalic Cordatns, 300. — Bothriocephalus Cristatus, 300. — Bothrio- 
cephalus Liguloides, 300. 

Nematodes, or Round=worms, 300. — Ascaris Lumbricoides, 300. 
— Ascaris Mystax, 301. — Ascaris Maritima, 301. — Oxyuris Vermicu- 
laris, 301. — Trichina Spiralis, 302. — Ankylostoma Duodenale, 303. — 
Anguillula Intestinalis and Stercoralis, 304. — Trichocephalus Dispar, 
304. — Filaria Medinensis, 305. — Filaria Sanguinis Hominis, 306. — 
Other Forms of Filaria, 307.— Echinococcus Gigas, 307. — Eustrongylus 
Gigas, 308. — Strongylus Longevaginatus, 308. 

Trematodes, or Fluke=worms, 308. — Distoma Hepaticum, 308. — 
Distoma Lanceolatum, 309. — Distoma Hematobium, 309.— Distoma Pul- 
monale, 310. — Other Fluke-worms, 310. 

Annelids, 310. 

Arthropodia, 311. — Pentastomum Denticulatum, 311. — Myiasis, 311. 



PART II. — SPECIAL PATHOLOGY. 



CHAPTER I. 

Diseases of the Blood 312 

Anatomy, 312. — Blood formation, 317. — Pathologic Changes in Eed 
Corpuscles, 317. — Pathologic Changes in Leukocytes, 319. — Pathologic 
Changes in Plasma, 320.— Plethora, 320.— Oligemia, 321.— Hydremia 
and Anhydremia, 321. — Lipemia, 322. — Melanemia, 322. — Hemocytol- 
ysis and Hemoglobinemia, 323. — Polycythemia, 324. — Leukocytosis, 
324.— Hypoleukocytosis, 326.— Anemia, 327.— Chlorosis, 329.— Pro- 
gressive Pernicious Anemia, 331. — Leukemia, 333. — Hodgkin's Disease, 

337. — Pseudoleukemia Infantum, 337. — Foreign Bodies and Parasites, 

338. — Methods of Examining the Blood, 338. 



CHAPTER II. 

Diseases of the Lymphatic Tissues 340 

Spleen, 340. — Abnormal Development and Situation, 341. — Circu- 
latory Disturbances, 342. — Inflammation, 343. — Atrophy and Degenera- 
tion, 345. — Tumors and Parasites, 346. — Infectious Diseases, 347. 



12 



CONTENTS. 



Lymphatic Glands, 348— Atrophy, 348.— Hypertrophy, 348.— 
Degenerations, 348. — Inflammation, 350. — Infectious Diseases, 352. — 
Tumors, 355. 

Bone=marrow, 357. — Degenerations, 357. — Atrophy, 358.— Hyper- 
trophy, 358. Inflammation, 358. — Infectious Diseases and Tumors, 
359. 

Thymus Gland, 359. 



CHAPTEE III. 

Diseases of the Circulatory System 360 

Heart, 360. — Congenital Diseases and Deformities, 360. — Circulatory 
Disturbances, 364. — Endocardium, 366. — Endocarditis, 366. — Circulatory 
Disturbances, 374. — Degenerations, 374. — Inflammation, 379. — Hypo- 
plasia and Atrophy, 385. — Hypertrophy and Dilatation, 387. — Aneurysm, 
390. — Wounds and Rupture, 390. — Infectious Diseases, 391. — New- 
Growths and Parasites, 391. — Pericardium, 391. — Circulatory Disturb- 
ances, 392. — Inflammation, 392. — Infectious Diseases, 396. — Tumors and 
Parasites, 396. — Pneumopericardium, 396. 

Arteries, 397.— Congenital Defects, 397.— Hypertrophy, 397.— 
Atrophy, 397. — Degenerations, 398. — Inflammation, 399. — Infectious 
Diseases, 404. — Aneurysm, 404. 

Veins, 411. — Circulatory Disturbances, 411. — Degenerations, 412. — 
Inflammation, 411. — Dilatation, 413. — Tumors, 414. — Infectious Dis- 
eases, 415. 

Lymphatic Channels, 415.— Inflammation, 415.— Dilatation, 415. 
— Infectious Diseases, 416. — Tumors, 416. — Parasites, 417. 
Thoracic Duct, 417. 



CHAPTER IV. 

Diseases of the Respiratory System 418 

Nasal Cavities, 418.— Congenital Abnormalities, 418.— Circulatory 
Disturbances, 418. — Inflammation, 418. — Infectious Diseases, 419. — 
Tumors, 419. — Parasites and Foreign Bodies, 420. 

Larynx, 420.— Congenital Abnormalities, 420.— Circulatory Dis- 
turbances, 420. — Inflammations, 421. — Infectious Diseases, 422. — 
Tumors, 423. — Parasites and Foreign Bodies, 424. 

Trachea, 424.— Malformations, 424. — Circulatory Disturbances, 424. 
— Inflammation, 424. — Infectious Diseases, 425. — Tumors, 425. 

Bronchi, 425. — Congenital Malformations, 425. — Circulatory Dis- 
turbances, 425. — Inflammations, 425. — Stenosis and Obstruction, 428. — 
Dilatation, 428. — Infectious Diseases, 429. — Tumors, 429. — Parasites 
and Foreign Bodies, 429. 

Lungs, 430.— Congenital Defects, 431. — Circulatory Disturbances, 
431. — Hypertrophy and Atrophy, 435. — Emphysema, 435. — Atelectasis, 
439.— Inflammation or Pneumonia, 441. — Gangrene, 458. — Tubercu- 



CONTENTS. 



13 



losis, 459. — Syphilis, 470. — Glanders, 472. — Actinomycosis, 472. — 
Tumors, 473. — Parasites, 475. 

Pleura, 476. — Circulatory Disturbances, 476. — Inflammation, 477. — 
Infectious Diseases, 481. — Tumors and Parasites, 482. 

CHAPTER V. 

Diseases of the G astro-intestinal Tract 484 

Mouth, 484. — Congenital Abnormalities, 484. — Circulatory Disturb- 
ances, 484. — Inflammation, 484. — Atrophy and Degeneration, 488. — 
Infectious Diseases, 488. — Tumors, 490. 
Teeth, 490. 

Pharynx and Tonsils, 492.— Circulatory Disturbances, 492. — In- 
flammations, 492. — Pressure-necrosis, 495. — Infectious Diseases, 496. — 
Tumors, 497. 

Salivary Glands, 498. 

Esophagus, 499.— Congenital Defects, 499.— Circulatory Disturb- 
ances, 499. — Inflammations, 499.— Stenosis, 500. — Dilatation, 500. — 
Perforation and Rupture, 501. — Infectious Diseases, 501. — Tumors, 501. 

Stomach, 502. — Congenital Defects, 502. — Circulatory Disturbances, 
502. — Inflammations, 503. — Peptic Ulcer, 506. — Atrophy and Degener- 
ations, 508. — Alterations in Position and Size, 508. — Infectious Dis- 
eases, 510. — Tumors, 510. 

Intestines, 514. — Abnormalities, 514. — Intestinal Obstruction, 517. 
— Prolapse of Rectum, 519. — Atrophy and Degeneration, 519. — Circu- 
latory Disturbances, 520.— Inflammation, 521. — Inflammation of Special 
Parts, 523. — Infectious Diseases, 527. — Tumors, 533. — Parasites, 536. — 
Intestinal Rupture and Foreign Bodies, 537. 

Liver, 538. — Malformations and Changes of Position, 538. — Circu- 
latory Disturbances, 539. — Atrophy and Degenerations, 541. — Inflam- 
mations, 546. — Hypertrophy, 551. — Rupture, 551. — Infectious Diseases, 
551. — Tumors, 553. — Parasites, 556. 

Biliary Ducts and GalNbladder, 558.— Inflammations, 558.— 
Stenosis and Dilatation, 559.— Gall-stones, Cholelithiasis, 560. — Tumors, 
561. — Jaundice, 561. 

Pancreas, 563. — Congenital Abnormalities, 563. — Circulatory Dis- 
turbances, 563. — Atrophy and Degenerations, 563. — Inflammations, 565. 
— Infectious Diseases, 566. — Tumors, 566. — Pancreatic Duct, 567. 

Peritoneum, 568. — Congenital Abnormalities, 568. — Circulatory 
Disturbances, 568. — Inflammations, 570. — Infectious Diseases, 573. — 
Tumors, 574. — Parasites, 575. 

CHAPTER VI. 

Diseases of the Ductless Glands 575 

Thyroid Gland, 575. — Congenital Defects, 576. — Disturbances of 
Circulation, 576. — Inflammations, 576. — Struma or Goiter, 576. — Infec- 
tious Diseases, 579. — Tumors and Parasites, 580. — General Results of 
Thyroid Disease, 580. 



14 



CONTENTS. 



Suprarenal Bodies, 582.— Congenital Anomalies, 582— Degenera- 
tions, 582. — Infectious Diseases, 583. — Circulatory Disturbances, 583. — 
Inflammation, 584. — Tumors, 584. — General Effects of Suprarenal Dis- 
eases, 584. 

CHAPTEK VII. 

Diseases of the Urinary Organs 585 

Kidneys, 585. — Congenital Anomalies, 585. — Changes of Position, 

586. — Circulatory Disturbances, 586. — Inflammations, 588. — Nephritis, 

588. — Chronic Nephritis, 593. — Chronic Parenchymatous Nephritis, 593. 

— Chronic Interstitial Nephritis, 595. — Atrophy and Hypertrophy, 603. 

— Degenerations, 604. — Concretions in the Uriniferous Tubules, 607. — 

Infectious Diseases, 608. — Tumors, 608. — Parasites, 612. 
Pelvis of Kidney and Ureter, 613. — Congenital and Acquired 

Malformations, 613. — Calculus, 614. — Inflammation, 614. — Infectious 

Diseases, 615. — Tumors, 616. — Parasites, 616. 

Urinary Bladder, 617. — Malformations, 617.— Changes of Position, 

617. — Rupture, 618. — Circulatory Disturbances, 618. — Inflammation, 

618. — Infectious Diseases, 620. — Calculi and Foreign Bodies, 621. — 
Tumors, 622. — Abnormal Conditions of the Urine, 624. — Chemical 
Changes and Sediments of Urine, 629. 

Urethra, 632.— Congenital Abnormalities, 632.— Inflammations ; 632. 
— Injuries, 635. — Infectious Diseases, 635. — Tumors, 636. 



CHAPTER VIII. 

Diseases of the Reproductive Organs 636 

Uterus, 636. — Development and Anatomy, 636. — Congenital Abnor- 
malities, 637. — Alterations of Position, 638. — Stenosis, Dilatation, and 
Rupture, 640. — Circulatory Disturbances, 641. — Inflammations, 642. — 
Infectious Diseases, 646. — Atrophy and Degenerations, 649. — Hyper- 
trophy and Hyperplasia, 649. — Tumors, 650. — Parasites, 655. 

Ovaries, 655. — Development and Anatomy, 655. — Congenital Ab- 
normalities, 656. — Changes in Position, 656. — Circulatory Disturbances, 
656. — Inflammation, 657. — Infectious Diseases, 657.— Tumors, 658. — 
Cysts of the Parovarium, 661.— Cysts of Kobelt, 662. 

Fallopian Tubes, 662.— Congenital Abnormalities, 662.— Changes 
of Position, 662.— Stenosis, 663.— Dilatation, 663.— Circulatory Disturb- 
ances, 663. — Inflammations, 664. — Infectious Diseases, 666. — Tumors, 
667. — Extra-uterine Pregnancy, 668. 

Vagina, 670.— Prolapse of Vaginal Wall, 670.— Stenosis, 670.— 
Wounds and Fistula?, 670. — Circulatory Disturbances, 671. — Inflamma- 
tions, 671.— Infectious Diseases, 672. — Tumors, 672. 

Decidua, Placenta, and Fetal Membranes, 672— Anatomic 
Considerations, 672. — Abnormalities of Development, 673. — Circulatory 
Disturbances, 673.— Inflammation, 674. — Infectious Diseases, 675. — 
Hyperplasia, 675. 



CONTENTS. 



15 



Vulva, 677.— Wounds, 677. — Circulatory Disturbances, 677. — Inflam- 
mation, 677. — Infectious Diseases, 678. — Tumors, 678. 

Penis and Scrotum, 679.— Congenital Abnormalities, 679. — In- 
flammation, 679. — Infectious Diseases, 680. — Tumors, 680. — Injuries, 
681. 

Testicles, 681. — Congenital Abnormalities, 681. — Atrophy and 
Hypertrophy, 681. — Degenerations, 682.— Circulatory Disturbances, 
682. — Inflammation, 682. — Infectious Diseases, 685. — Tumors, 687. — 
Parasites, 689. 

Prostate Gland, 689. — Inflammation, 689. — Atrophy and Degener- 
ation, 690. — Concretions, 690. — Infectious Diseases, 690. — Hypertrophy 
and Tumors, 690. 

Cowper's Glands, 693. 

Seminal Vesicles, 693. 

Mammary Glands, 694— Congenital Abnormalities, 694.— Circu- 
latory Disturbances, 694. — Inflammations, 695. — Atrophy and Hyper- 
trophy, 696. — Degenerations, 696. — Infectious Diseases, 696. — Tumors, 
697. 

CHAPTER IX. 

Diseases of the Bones 700 

Anatomy and Development, 700. — Pickets, 701. — Regeneration of 
Bone, 703. — Circulatory Disturbances, 706. — Inflammations, 706. — 
Hypoplasia and Atrophy, 710. — Degenerative Conditions, 710. — Infec- 
tious Diseases, 712. — Tumors, 716. 



CHAPTER X. 

Diseases of the Joints 718 

Luxation and Ankylosis, 718 — Distortion, 718. — Circulatory Disturb- 
ances, 718. — Inflammations, 719. — Infectious Diseases, 722. — Tumors, 
723. — Tendon-sheaths and Bursse, 724. 



CHAPTER XI. 

Diseases of the Voluntary Muscles 724 

Hypertrophy, 724. — Circulatory Disturbances, 725. — Inflammations, 
725. — Atrophy and Degenerations, 727. — Infectious Diseases, 730. — 
Tumors and Parasites, 730. 



CHAPTER XII. 

Diseases of the Brain and its Membranes 731 

Dura Mater, 731. — Circulatory Disturbances, 731.— Inflammations, 

731.— Infectious Diseases, 732.— Tumors, 733.— Cysts, 733. 

The Pia and Arachnoid, 734.— Circulatory Disturbances, 734. — 

Inflammation, 735. — Infectious Diseases, 738. — Tumors, 740. 



1(3 



CONTENTS. 



Brain, 742. — Development and Anatomy, 742. — Congenital Abnor- 
malities, 748. — Post-mortem Degenerative Conditions, 751. — General 
Pathologic Anatomy of the Nervous System, 752. — The Blood-vessels, 
764. — Circulatory Disturbances, 766. — Inflammation, 775. — Injuries to 
Central Nervous System, 783. — Infectious Diseases, 784. — Choroid 
Plexus and Ventricles, 761. — Tumors, 785. — Choroid Plexus, 788. — 
Ventricles, 791. — Pituitary Body, or Hypophysis Cerebri, 794. — Pineal 
Gland, or Epiphysis Cerebri, 798. 

CHAPTEE XIII. 

Diseases of the Spinal Cord and its Membranes 798 

Dura Mater, 798. — Fatty Infiltration, 798— Hemorrhage, 798. — 
Tuberculosis, 799.— Syphilis, 799. 

Pia and Arachnoid, 800. — Circulatory Disturbances, 800. — Degener- 
ations, 800. — Inflammations, 800. — Infectious Diseases, 801. 

Cord, 802. — Anatomy of the Cord, 802. — Congenital Abnormalities, 
804. — Hydromyelia and Syringomyelia, 805. — Circulatory Disturbances, 
808. — Inflammations, 811. — Primary Degenerations, 817. — Secondary 
Degenerations, 825. — Tumors, 827. 

CHAPTEE XIV. 

Diseases of the Peripheral Nervous System 827 

Ganglia of the Cranial Nerves, 827. 

The Nerves, 828. — Circulatory Disturbances, 828. — Atrophy and 
Degeneration, 828. — Eegeneration after Injury of Nerve, 829. — Inflam- 
mation, 831. — Infectious Diseases, 833. — Tumors, 834. 



A TEXT-BOOK OF PATHOLOGY. 



PART I. 
GENERAL PATHOLOGY. 



Pathology is the science that deals with disease in all its 
aspects. It includes the study of the causes, the manifestations, 
and the results of disease. 

Three important subdivisions of the study of pathology are 
recognized, viz., etiology, or the study of the causes of disease; 
morbid or pathologic anatomy, the study of the structural changes 
in disease ; and morbid or pathologic physiology, the study of 
disturbances of function. In the latter group is included patho- 
logic chemistry, as morbid chemical action and its results are the 
outcome of disturbed function. 

Pathology may be divided into general and special pathology. 
The former treats of causes of disease and pathologic processes 
irrespective of any individual part; the latter deals with the causes 
or processes in individual diseases, organs, or parts. 

Disease itself may be defined as abnormality in structure, in 
function, or in both combined. It is doubtful whether alteration 
of function can occur without some alteration in structure, but it 
frequently happens that functional disturbances are present though 
no structural alterations are discoverable even by the most precise 
methods of investigation. 

The symptoms of disease are the expressions of abnormal func- 
tional activity, and are therefore properly discussed under the 
head of pathologic physiology ; but they are so important from a 
practical standpoint, and form such an extensive subject of inves- 
tigation, that they are usually considered apart from pathology, 
in special treatises dealing with diagnosis and the practice of 
medicine. 



2 



17 



18 



TEXT-BOOK OF PATHOLOGY. 



CHAPTER I. 

THE ETIOLOGY OF DISEASE. 

The causes of disease may be classified as predisposing and 
determining. The former prepare the system or part by rendering 
it weaker and less resistant ; the latter are the immediate or spe- 
cific causes of disease. 

Predisposing" Causes. — The normal system is able to cope 
with the determining causes of disease to a certain point by its 
general vitality and regulative functions. Thus heat and cold 
may prove harmless if not too intense or prolonged. In the case 
of exposure to heat, the superficial capillaries become dilated, 
sweating increases, and there is increased heat dissipation from 
the surface at the same time that increased respiratory function 
occasions evaporation and loss of heat through the lungs. In 
the case of exposure to cold, increased muscular exercise leads to 
greater heat production, while contraction of the superficial blood- 
vessels restricts the elimination of heat. When, however, a cer- 
tain point of intensity is reached in the case of heat, cold, or other 
causes of disease, the normal organism is unable to oppose suffi- 
cient resistance, and disease or injury results. The degree of 
resistance differs in different individuals, in different races, or 
people living under varying climatic conditions, etc. In some 
the degree of resistance may be so great that certain diseases are 
never contracted. The term immunity (q. v.) is applied to this state. 
In other persons there is a recognizable weakness of resistance in 
one direction or another which constitutes a definite predisposition. 
The latter may be either hereditary or acquired. Acquired pre- 
disposition results from previous disease, vices of living, and like 
causes. 

Heredity as a predisposing factor in disease is probably less 
important than was formerly believed, but undoubtedly plays a 
part in many conditions. By hereditary predisposition is desig- 
nated abnormal weakness of resistance transmitted from the mother 
or father to the offspring. There may be congenital weakness 
that is not definitely hereditary, as it is more or less accidental — 
that is, not the outcome of tendencies of the same kind (latent or 
active) in the parent. Heredity may be direct or immediate — 
that is, from the parent (himself or herself presenting the condi- 
tion) to the offspring — or remote, as in cases in which the hereditary 
trait is latent in the parent. One or several generations may thus 
be free from certain diseases or tendencies which reappear in 
later generations. This return to conditions present in remote 
ancestors has been likened to atavism in the Darwinian sense. In 
some cases hereditary traits are conveyed from the male parent to 
the male children, or from the female parent to the female off- 



THE ETIOLOGY OF DISEASE. 



19 



spring ; in other cases there is crossed transmission. A peculiar 
form of heredity is seen in hemophilia and some other diseases, 
which are transmitted through the female members of a family, 
who generally remain unaffected, to the male offspring. Heredi- 
tary traits sometimes predispose to a number of allied affections. 
This is particularly striking in the case of the neuropathic heredity, 
in which various forms of nervous disease may appear alternately 
or irregularly in members of an affected family. 

A number of theories have been constructed to explain the mechanism 
of heredity. Darwin in his hypothesis of pangenesis suggested that minute 
particles are given off from all of the cells of the body ; these are collected 
in the reproductive cells, which in consequence represent all of the bodily 
characteristics, hereditary and acquired. Weismann denied the transmis- 
sibility of acquired characteristics, and holds that in the process of reproduc- 
tion a certain amount of "germ-plasm" passes from the parent cell into 
the offspring, where it remains, and is in turn passed on to succeeding genera- 
tions, thus perpetuating ancestral characteristics. 

Determining Causes. — Among the immediate or deter- 
mining causes of disease are those which originate outside the 
body and those which are generated within the body. Among 
the former are included traumatism, heat, cold, and other physical 
agents, poisons, and living organisms, including bacteria and va- 
rious animal parasites. The causes of disease originating within 
the body itself are less definitely known, but it has been found in 
chemical studies that various products of normal metabolism when 
accumulated in abnormal quantity, or products of disturbed metab- 
olism, may occasion local or widespread disease of various sorts. 
This self-poisoning is designated auto-intoxication. 

The term "auto-intoxication" is frequently applied to poisoning by 
products of intestinal putrefaction. This application of the term is not, 
strictly speaking, correct. The same poisons might have been produced by 
putrefaction of food outside the body, when the use of the name auto-intoxi- 
cation would be manifestly absurd. If poisons are produced by imperfect 
digestion, and these affect the organism, the condition could properly be 
termed auto-intoxication. 



TRAUMATISM. 

Traumatism, or mechanical injury, may be of various sorts, 
gradual or sudden, small or large ; and the effects are dependent 
upon the form and severity of the injury. Pressure brought to 
bear upon a part leads to disturbances of the circulation and more 
or less direct injury of the cellular elements. When the pressure 
is gradual true atrophy of the part may occur, as in the case of the 
atrophic liver resulting from lacing. When the pressure is greater 
and the circulation is completely arrested more destructive change 
may result, such as necrosis or gangrene. This is seen in the 
necrotic atrophy of bone resulting from the pressure of aneurysms, 



20 



TEXT-BOOK OF PATHOLOGY. 



or the gangrene of extremities resulting from ligation. Wounds. 
— Frequently, inflammatory reaction occurs in the surrounding 
tissues when traumatic injuries have been sustained. This is 
illustrated in all forms of wounds, and it is through the inflam- 
mation and subsequent regeneration of tissue that the areas of 
destruction are restored. In cases of injury by fine particles, as 
in powder-marks of the skin, or the surface injuries sustained by 
miners and metal-AVorkers, or in individuals inhaling sharp par- 
ticles like coal-dust, marble-dust, or steel-filings, small injuries of 
the tissues result. The foreign bodies may be subsequently dis- 
charged, leaving a focus of inflammation, or the inflammation may 
surround the particle imbedded in the tissue, and encapsulation by 
fibrous-tissue formation may occur. Large injuries in which the 
tissues are contused or broken may lead to extensive inflamma- 
tion, in part the result of the direct injury to the tissues and in 
part the result of injury of the blood-vessels. 

Gross traumatism of the body as a whole, as in falls, crushing 
injuries, etc., causes various disturbances according to the part 
mainly involved. Rupture of the viscera, as the lungs, heart, 
liver, spleen, stomach, or intestines, may occur. When the head is 
violently struck, unconsciousness is common as a consequence 
of either disseminated punctiform hemorrhages, large focal hem- 
orrhages, or obscure and possibly only functional disturbances. 
Commotio cerebri, the condition occurring in such cases, may be 
fugacious or may lead to permanent disorder dependent upon 
organic changes in the brain. Spinal symptoms, met with after 
railway injuries and like accidents, may be due to hemorrhage 
and secondary morbid processes in the cord, or may be due to the 
uncertain pathologic conditions constituting hysteria. 

PHYSICAL CONDITIONS. 

Heat. — High temperatures produce local or general results 
according to the mode of application and degree of heat. 

Local excess of heat produces various lesions. Moderate excess 
leads to relaxation of the walls of the blood-vessels ; with increas- 
ing grades of temperature there is in addition necrotic change in 
the cells of the part, and exudation of serum causes vesicle for- 
mation. Still higher grades of temperature produce immediate 
destruction, perhaps with charring, of large or small areas, while 
the surrounding tissues suffer from reactive inflammation and 
hyperemia. Extensive burns involving one-third or more of the 
surface of the body frequently cause death. In these cases it is 
likely that poisonous products are formed, either directly through 
tissue- and blood-destruction, or indirectly through disturbances 
of the functions of the skin or internal organs. The immediate 
manner of death is often in the form of shock ; when the termi- 



THE ETIOLOGY OF DISEASE. 



21 



nation is more delayed various vascular, hemic, and tissue-disturb- 
ances may occur. Intravascular coagulation is not unusual, and 
is not improbably the result of the liberation into the blood of 
tissue-elements set free in the areas of local destruction, or to sub- 
stances produced by direct destruction of the blood. The same 
substances may account for the existence of fever (ferment intoxi- 
cation). The intravascular coagulation caused in this or other 
ways may induce venous stasis and localized hemorrhages. Focal 
necrosis or degeneration of the tissues of various organs, such as 
the liver, kidneys, or the mucous and serous membranes, may be 
due to thrombotic occlusion of vessels, or to the influence of cir- 
culating poisons without thrombosis, or to both. Duodenal ulcer 
is often referred to as an occasional result of extensive burns. 
The blood itself may present evidence of disease in the form of 
degenerations of the corpuscles, in the reduction of their number 
and of the amount of coloring matter ; while regenerative changes 
frequently present themselves some time later (nucleated red cor- 
puscles). Changes in the urine may occur in cases of extensive 
burns, in consequence of the tissue-destruction (hemoglobinuria, 
albumosuria). 

Exposure to general high temperature varies in its effects accord- 
ing to the manner of exposure (dry air, steam, etc.). An animal 
exposed to a constant temperature somewhat above the usual 
surrounding temperature presents a slight increase of its body- 
heat, which is compensated for by increase in the respirations 
and pulse-rate. Much higher temperatures may cause death 
by coagulation of the tissues ; notably, the muscular struct- 
ure of the heart, or the respiratory muscles. Before this extreme 
is reached, however, it may be found that the consumption of the 
tissues of the body is greatly in excess, though the respiratory 
quotient is altered in favor of the amount of air inhaled. Con- 
tinuous exposure to excessive heat frequently causes peculiar dis- 
turbances in man, known as heatstroke, sunstroke, or insolation 
and heat-exhaustion. In these conditions hyperemia and edema, 
or even inflammation of the meninges, may occur. These lesions 
are sometimes supposed to be the result of the direct effect of 
the heat; but there is reason to believe that they may be occa- 
sioned by poisonous substances produced within the body by dis- 
turbed metabolism, as a result of the heat. 

A portion of the body, as an arm or a leg, may be exposed for a 
limited time to excessive temperatures (300° to 400° F.) in dry 
air without injury. The general temperature is slightly elevated, 
but metabolism is practically unaffected. 

The effects of general or local heat are much increased when the organ- 
ism as a whole or in the part involved is below par. A paralyzed limb is 
burned or scalded at comparatively low temperatures. 



22 



TEXT-BOOK OF PATHOLOGY. 



Cold. — Exposure to extreme degrees of cold may cause results 
quite similar to those produced by heat. Exposure of the skin to 
liquefied air, solidified mercury, or other substances at excessively 
low temperatures produces vesiculation and necrosis of the tissues 
like those produced in burns. 

Exposure of the body to greatly reduced but bearable tempera- 
tures of the surrounding atmosphere causes vascular disturbances 
followed by necrosis of the tissues and inflammatory changes. 
The parts so affected are the extremities or projections of the 
body, like the toes and fingers, nose and ears. The primary 
result of cold is vascular constriction aiid local anemia. These 
serve the purpose of preserving the body heat by preventing heat 
radiation ; later the blood-vessels are paralyzed and extreme hyper- 
emia results. Then cellular exudation and necrosis may occur. 
These changes are well seen in the condition termed chilblain. 
In prolonged exposure to cold there are a gradual reduction in 
the activity of the various organs and a gradual obtunding- of 
the sensibility till the patient becomes comatose. The retention 
of excrementitious products of metabolism, or the formation of 
products of abnormal metabolism, may be important in causing 
this condition. 

Exposure to cold plays an important part as a clinical cause of 
disease. Various forms of pharyngitis and coryza or bronchitis 
so frequently follow such exposure that the term " cold " is gener- 
ally used. Other conditions, like rheumatism, pleurisy, pneumonia, 
and the like, bear a similar relation. It is now recognized that in 
most of these cases cold is merely a predisposing cause, the imme- 
diate cause being in many, if not all, cases specific micro-organ- 
isms. The mode of action of the exposure is uncertain ; probably 
it causes a reduction in the resisting powers of the organism and 
thus favors the activity of bacteria. In some cases it may be that 
the cold alters the fluids of the body in such a Avay as to permit 
increased virulence of micro-organisms already present, or to pro- 
mote their entrance into the system. 

Increased Atmospheric Pressure. — Exposure to extreme 
pressure of several atmospheres may occur among deep-sea divers, 
or in men working in caissons used in bridge building. But little 
disturbance may be caused at first, or for a long time ; but on 
return of the workmen to the usual atmospheric conditions symp- 
toms make their appearance (caisson disease). Among these symp- 
toms are bleeding from the nasal or other mucous membranes, 
great depression, delirium, and paralytic conditions. Congestion, 
degenerations, and vacuolations in the spinal cord have been dis- 
covered in some cases. 

Decreased Atmospheric Pressure.— Effects of decreased 
pressure are seen in inhabitants of high altitudes and in persons 
ascending in balloons. Marked excitement of the vascular system, 



THE ETIOLOGY OF DISEASE. 



23 



hemorrhages, somnolence, weakness, vomiting, and similar symptoms 
are observed ; in less marked cases a general excitement of the 
nervous system, sleeplessness, etc., occur. These symptoms have 
been attributed to lack of oxygen, and compressed air and oxygen 
have been successfully used to combat them ; but experiments 
show that the air-pressure may be as low as 400 mm. of mercury 
without interference with the respiratory exchange of gases. To 
a certain extent the symptoms are probably mechanical and due 
directly to the reduced pressure on the exterior. Recent studies 
show that the blood contains greatly increased numbers of red 
corpuscles in a gi ven volume, and the percentage of hemoglobin is 
correspondingly increased. This is probably due, to a large extent, 
to disturbance in the distribution of the corpuscles with stagnation 
in the peripheral vessels (see Diseases of the Blood). 

Insufficiency of Respiratory Air. — A certain amount of 
air is necessary for the continuance of health or life. Insufficiency 
may be due to diseases which obstruct the air-passages or affect 
the pulmonary tissue itself, and to foreign bodies (solid bodies, water 
in drowning) within the air-passages. Changes in the atmosphere 
or gases taken into the lung may cause insufficiency in the supply 
of oxygen, notably in CO-poisoning, in which the foreign gas enters 
into firm combination with the hemoglobin of the blood and thus 
excludes oxygen. 

Moderate decrease of the supply of air causes labored and rapid 
breathing, more or less cyanosis, depression, and stupor. This 
condition is termed asphyxia. Complete lack of air causes increase 
of these symptoms and death by suffocation. In these cases the 
blood is exceedingly dark and fluid, and hemorrhages may be 
found in various situations. The latter result from excessive blood- 
pressure during the death agony. Long-continued insufficiency 
of oxygen may directly or indirectly occasion degenerative dis- 
eases of the tissues. 

It has often been asserted that anemia causes many of its symptoms and 
results because the blood is incapable of carrying sufficient oxygen in its 
reduced state. As a matter of fact, however, physiologic experiments 
have demonstrated that the respiratory exchange (inhalation of oxygen and 
exhalation of carbonic acid gas) is but little affected and is as frequently 
increased as decreased. 

Electrical Influences. — Electrical discharges may cause 
burns or similar lesions of the surface, and frequently cause intense 
shock. Disturbances of the central nervous system of various sorts 
may occur immediately or some time after the exposure. Doubt- 
less there are distinct organic changes in the nervous tissues, but 
these have not been determined. Gross injuries of organs, such 
as rupture and degenerative changes, may be occasioned. 



24 



TEXT-BOOK OF PATHOLOGY. 



POISONS. 

Definition. — The term poison may be applied to substances 
which when introduced in relatively small amounts into the living 
organism disturb its structure or functional activity. 

The Action of Poisons in General. — Gaseous poisons act 
primarily upon the respiratory mucous membranes with which they 
come in contact, or after absorption into the blood disorganize this 
fluid or lead to disturbances of the nervous system. Liquid poi- 
sons are generally absorbed through the gastro-intestinal mucous 
membrane, but may be received directly into the tissues by injec- 
tion under the skin. They are rarely absorbed through the skin. 
Solid poisons must in all cases first be dissolved, and are then ab- 
sorbed like the liquid poisons. They may by their strong attrac- 
tion for water absorb the latter directly from the tissues, and by 
this process alone may bring about important changes. 

The lesions due to a poison may be entirely local, as in the 
case of certain corrosives or caustics ; in other cases the point of 
entrance is unaffected, the pathologic manifestations being en- 
tirely due to the changes in different parts of the body, or to ner- 
vous disturbances resulting from the circulation of the poison in 
the blood. 

The fate of poisons after ingestion is very different in dif- 
ferent cases. Some poisons circulate with the blood and are 
eliminated unchanged. Others may suffer chemical change within 
the stomach or other cavities of the body before absorption, and 
may be either completely neutralized, or may be converted into 
forms which are subsequently slowly absorbed. After absorption 
into the blood other chemical reactions may occur, and the poison 
may be more or less neutralized, the system then suffering either 
from the resulting compounds or from the changed conditions of 
the blood. Active destruction of the poison may occur in the 
blood or in the various organs, especially the liver. In these 
processes, however, the glandular organs may suffer seriously, 
various forms of degeneration or necrosis resulting. 

The effect of poisons depends upon the dose as well as upon 
the nature of the substance, and also upon the individual. The 
repeated ingestion of certain poisons, such as arsenic or opium, 
may generate a considerable degree of immunity or tolerance 
(Mithridatization). Similar immunity may be characteristic of a 
given individual or of classes or species. Susceptibility to the action 
of poisons is further influenced by age and constitutional vigor. 
Children bear certain poisons better, comparatively speaking, than 
adults, while the reverse is true of other substances. Sometimes 
there are idiosyncrasies which lead to peculiar results not observed 
in the average individual. In consequence of this, substances ordi- 
narily not toxic may be extremely injurious to certain persons. 



THE ETIOLOGY OF DISEASE. 



25 



Sometimes poisons are comparatively innocuous when administered in 
one way, though powerfully toxic to the same animal when otherwise intro- 
duced. Thus in dogs intravenous injection of atropin is very slightly in- 
jurious, but injection into the spinal cord of minute doses causes rapid 
poisoning. It has been found that the leukocytes are concerned in the fixa- 
tion of the poison in the blood when intravenous injection is practised. 

Elimination. — The excretion of poisons may take place 
through the kidneys, lungs, the mucous membrane of the gastro- 
intestinal tract, the mammary glands, or through the skin. In 
some instances a poison is eliminated without change in the 
excreta ; in other cases it suffers complete change, and is not 
present at all in the excretions. The rate of elimination varies 
greatly, and is more or less dependent upon conditions of the 
system. Some poisons, as phosphorus and mercury, may be stored 
up within the body for a considerable period, subsequently suffer- 
ing slow elimination. 

Classification. — The number of substances which may act as 
poisons is very great, and the manifestations are of very different 
sorts. Classification of poisons is therefore difficult and not en- 
tirely satisfactory. We may crudely distinguish between gaseous, 
liquid, and solid poisons ; between animal and vegetable, organic 
and inorganic, and the like ; but these classifications have no 
scientific value. 

From the point of view of the action of the poisons we may 
distinguish corrosive poisons, or those which have a local action ; 
organic ov parenchyma-poisons, or those which act less strongly at 
the point of application than upon the various organs to which 
they are conveyed through the blood ; blood-poisons, or those 
which exercise their eifects primarily upon the blood ; and the 
nerve-poisons, or those which disturb the functional activity of the 
nervous system without producing definitely discoverable lesions. 

Corrosive Poisons ; Escharotics ; Caustics. — Under this heading 
are included various acids, alkalies, and mineral poisons, such as 
sulphuric, nitric, oxalic, carbolic, and hydrofluoric acids, caustic 
potash or soda and ammonium, and gases like chlorin and bromin. 
Xitrate of silver, bichlorid of mercury, sulphate of copper, and 
other inorganic compounds have a similar action, and certain 
organic bodies, such as canthariclin and croton oil, belong to the 
same class. 

All these poisons exercise a destructive effect upon the cells 
w T ith which they come in contact, partly by abstraction of water 
and partly as a result of a coagulating power or similar action. 
The acids and mineral caustics usually produce dry and more or 
less discolored areas of necrosis ; the caustic alkalies cause a sort 
of gelatinous change or a saponification of the tissue. The degree 
of injury depends upon the poison and the amount in contact with 
the tissues. There may be only a superficial injury of the outer 



26 



TEXT-BOOK OF PATHOLOGY. 



layer of epithelial cells, or extensive destruction. Reactive inflam- 
mation is almost always present, and often, especially in the mucous 
membranes, the inflammatory reaction is extensive though the cor- 
rosive action of the poison is limited in depth and extent. The 
affected part may present slight areas of necrosis with reactive 
hyperemia and inflammation beneath and around them, or deep 
eschars, vesicles, or large bulla?. In the process of healing 
extensive scars may form, and these may be serious in their effects, 
as in the case of strictures of the esophagus. 

Organic Poisons ; Parenchyma-poisons. — This large group in- 
cludes many metallic compounds that have a local corrosive or 
escharotic effect, but which may in smaller dose gain entrance to 
the blood and cause extensive organic lesions. It also includes 
poisons of vegetable origin and products of bacterial growth. In 
general these poisons have a similar action. The kidneys and the 
mucous membrane of the intestines are especially active in their 
elimination and suffer most seriously. Degenerations of the epithe- 
lial cells of various sorts are met with, such as nuclear degenera- 
tions, coagulation necrosis, fatty degeneration, and even calcifica- 
tion. The changes may be diffuse or may occur in small foci. In 
the latter case small areas of granular appearance, having a lighter 
color than the surrounding tissues, are seen ; and on staining the 
cells are found to color poorly or not at all, the nuclei often show- 
ing this change first. Nuclear degenerations (fragmentation, hyper- 
chromatosis, etc.) are observed, and in some instances marked fatty 
degeneration of the cells occurs. Around the foci of degeneration 
there is more or less round-cell infiltration (polymorphonuclear 
cells), and to a less degree the degenerated area itself is infiltrated. 
In cases in which diffuse change occurs there is equally diffuse 
round-cell infiltration. After the acute process has subsided 
hyperplasia of the connective tissues may occur and the affected 
part becomes more or less sclerotic or indurated. Regeneration 
of the parenchyma-cells is less apt to occur. 

Some of the more important of the poisons of the group may 
now be separately considered. 

Phosphorus is a poison of considerable activity in the yellow 
form ; the red variety is inert. Workmen in match factories are 
the most frequent victims of this form of intoxication, but occa- 
sionally accidental poisoning by swallowing occurs. In the latter 
the manifestations are acute. The pathologic changes are catarrhal 
inflammation of the gastro-intestinal mucous membrane and more 
or less widespread fatty degeneration of various tissues and organs. 
The liver suffers most severely, being enlarged, light yellow or 
reddish in color, and friable or doughy. Microscopically the liver- 
cells are found extensively degenerated (fatty). Similar but less 
marked fatty degeneration is found in the renal tubules, gastro- 
intestinal epithelia, and heart-muscle, and in the intima of the 



THE ETIOLOGY OF DISEASE. 



27 



blood-vessels. Extensive jaundice is frequent and numerous 
hemorrhages may occur. In the more chronic poisoning of match- 
makers the poison enters through the mouth and respiratory pas- 
sages, being inspired as dust. Chronic catarrhal inflammation of 
the respiratory tract may occur and a peculiar form of necrosis of 
the bones (see Bones) is met with. 

Arsenic is poisonous in certain forms (white arsenic, arsenous 
acid) and inert in other forms (the sulphids). Acute poisoning 
occurs when toxic forms are swallowed in large doses ; the chronic 
forms of poisoning result from gradual ingestion or the inhalation 
of dust containing arsenic. Cases of the latter sort occur when 
wall-paper, hangings, and the like, colored with arsenic-pigments, 
are used. The lesions in acute arsenic-poisoning resemble those 
produced by phosphorus. The gastro-intestinal inflammation is, 
hoAvever, more severe ; while the fatty degeneration of the organs 
is less marked. In chronic arsenic-poisoning changes in the 
peripheral nerves (degeneration and inflammation) are most im- 
portant. It is likely that focal or diffuse myelitis may likewise be 
caused by this poison. Chronic inflammations of the gastro- 
intestinal or respiratory mucous membranes are met with in some 
cases. Inflammatory lesions and pigmentation of the skin may 
occur. 

Lead. — Among the compounds leading to acute or subacute 
poisoning the chromate, the acetates, the carbonate, and oxid are 
most important. Chronic poisoning occurs in workmen in paint 
manufactories and among painters, and in persons drinking certain 
waters that have been conducted through lead pipes. Less rarely 
the use of cosmetics, dyestuffs, etc., containing lead causes chronic 
poisoning. In the acute forms of lead-poisoning moderate gastro- 
enteritis occurs. In the chronic form changes in the nervous sys- 
tem are most important. Peripheral neuritis is the most frequent 
lesion, but changes in the large ganglionic cells of the gray matter 
of the cord have sometimes been found. Diffuse sclerosis of the 
blood-vessels, interstitial nephritis, and the lesions of gout may be 
present. Atrophy and fatty degeneration of the muscle-libers are 
less important lesions. A blue line on the gums at the junction 
with the teeth (due to deposit of sulphid of lead) is a lesion of 
clinical importance. 

Mercury. — Poisoning with mercury may be acute, subacute, or 
chronic. The first is due especially to the corrosive chlorid and 
other mercuric salts ; the second to calomel or small doses of those 
of the former group. Chronic poisoning occurs as a result of inhala- 
tion of fumes or dust containing mercury, and is seen in workmen 
in mirror manufactories. In the acute cases violent inflammatory 
and necrotic lesions of the gastro-intestinal tract are seen. Paren- 
chymatous degeneration, fatty change, and even calcification of the 
renal epithelium may occur ; and fatty degeneration in other 



28 



TEXT-BOOK OF PATHOLOGY. 



organs may sometimes be met with. In subacute cases marked by 
ptyalism some change is doubtless present in the salivary glands, 
but the nature of this has not been determined. 

Ergot. — Ergot is a poison capable of producing intense toxic 
results. It contains two important toxic principles, sphacelinic 
acid and an alkaloid, cornutin. Acute poisoning sometimes re- 
sults from overdosage ; while chronic intoxication occurs from 
the use of affected grain, particularly in famine years. Wide- 
spread poisoning of communities has sometimes resulted. The 
lesions produced are not definite or uniform. Gastro-intestinal 
inflammation and erosion of the mucous membrane have been ob- 
served, but are not habitual ; sclerotic change in the spinal cord 
has been found in a few cases. Gangrene is a frequent lesion, 
probably resulting from vascular obstruction due to contraction 
of the blood-vessels. Enlargement of the spleen has sometimes 
been noted. 

Toxalbumins from Plants. — Certain vegetable bodies, like 
riein derived from the castor bean and abrin derived from 
jequirity bean, are exceedingly toxic, acting in part as blood- 
poisons but also as parenchyma-poisons. Injected into animals 
these substances cause violent intoxication, and focal areas of 
necrosis in various situations, notably in the liver. In part these 
lesions result from vascular thrombosis ; in part from direct ac- 
tion. The study of the action of these poisons is of particular 
interest from the resemblance of the lesions to those caused by 
certain bacteria and bacterial poisons. 

Toxic Products of Bacteria. — In the growth and multiplica- 
tion of various bacteria definite toxic substances are produced, 
and through the latter the lesions of infection are to a large ex- 
tent produced. Such poisonous bodies may be generated in the 
growth of the bacteria outside of the body, as well as within the 
body. In the latter case the pathologic lesions at the point of 
infection may be the focus of origin of toxic substances which 
are then distributed throughout the body in the blood. This is 
eminently true of tetanus, and to a large degree of diphtheria. 
In other cases the bacteria themselves are transported to various 
parts of the body, and finding lodgement in the tissues set 
up changes by which their toxic products are evolved. The 
latter increase the local foci of pathologic change and then 
spread in the circulation and cause general intoxication. Fur- 
ther reference to these poisons will be made when discussing the 
individual bacteria. 

The venom of serpents and of various insects contains 
toxic bodies, some of which are albuminous in nature. These vary 
in their action, being to some extent blood-poisons, but more par- 
ticularly parenchyma-poisons. The lesions produced are local and 
general. Locally there are intense inflammatory reaction and 



THE ETIOLOGY OF DISEASE. 



29 



edema around an area of cellular necrosis or destruction where the 
poison has come in immediate contact with the tissues. The blood 
seems to suffer great disorganization and corpuscular change. 
Petechial hemorrhage and foci of cellular necrosis occur in various 
organs ; and edema of the lungs is frequently present. The action 
of the venom of different animals varies in kind and intensity to 
a certain extent, but is in general of a similar type. 

Blood-poisons. — Various liquid or gaseous substances are termed 
blood-poisons because of their especial action upon this liquid. 
The blood-poisons may be classified as (a) those which combine 
with the hemoglobin without changing the corpuscles ; (b) those 
which alter the red corpuscles and the coloring matter ; (c) those 
which affect the blood as well as the tissues generally ; and (d) 
those which cause changes in the blood-plasma, increasing or de- 
creasing the tendency to clotting. 

(a) Among the poisons which act by entering into combination 
with the hemoglobin without changing the corpuscles, carbon 
monoxid, cyanogen, and hydrogen sulphid are important. In 
carbon-monoxid poisoning, which often results from inhalation of 
the fumes of charcoal burning with insufficient air, the blood has 
a light color and light petechial discolorations may be seen in 
various parts of the body. In cyanogen-poisoning the blood is 
similarly light in color ; while in H 2 S-poisoning the blood is often 
dark, sometimes quite black. 

(6) Among the poisons which disorganize the blood-corpuscles 
and later the hemoglobin are a large number of chemical agents 
used in medical practice or in the arts, including potassium chlo- 
rate, nitroglycerin, anilin, nitrobenzol, various coal-tar derivatives, 
and arseniuretted hydrogen. Certain poisonous plants (toadstools) 
act similarly. These poisons lead to a reduction of the hemoglobin 
with formation of methemoglobin and at the same time destruc- 
tion of the corpuscles themselves, with release of the hemoglobin 
into the serum. The altered condition of the blood often induces 
secondary changes, such as fatty degeneration and hemorrhages in 
various organs. The blood-corpuscles are found in variously de- 
generated conditions, showing microcytosis and poikilocytosis in 
particular. Nucleated red corpuscles may be present as in other 
conditions of blood-destruction with attempted regeneration. 

(c) Among the poisons which disorganize the blood and at the 
same time cause changes in the parenchyma of organs, reference 
has been made to abrin and ricin. In addition to the organic 
changes, these substances cause certain alterations in the blood 
itself, increasing the coagulability and thus inducing thrombosis. 

(d) Various substances introduced in sufficient quantity are 
capable of affecting the plasma of the blood or the corpuscles in 
such a way as to affect its coagulability. Calcium salts, carbonic 
acid gas, and fibrin-ferment are active in this way, but the last 



30 



TEXT-BOOK OF PATHOLOGY. 



alone produces toxic results through this function. Ferment-in- 
toxication may occur in consequence of various other intoxications, 
when corpuscular or tissue-destruction has liberated the ferment. 
Among the poisons which decrease coagulability peptone (albu- 
mose) is important. 

Nerve-poisons. — This group contains a large number of sub- 
stances capable of producing violent symptoms and even death 
without definite change in the tissues of the body. Recent inves- 
tigations showing certain alterations in the finer structure of the 
nervous system in disease and in cases of intoxication suggest that 
histologic changes in the central neurons may be found to result 
from poisoning by these substances. Changes of this kind 
(changes in size and form of the cell and nucleus, thickening, con- 
traction, or disappearance of dendrites, alterations in the chromo- 
philic bodies, etc.) have been described in the gray matter of 
animals poisoned with alcohol and certain toxins of bacterial 
origin. It is not unlikely that similar changes will be found in 
other conditions. 

Among the nerve-poisons are alcohol, chloroform, ether, and 
various alkaloids like morphin, atropin, etc. In this same group 
might be included some of the poisons contained in the venom of 
serpents and other animals, but these usually cause definite 
lesions in the blood or tissues of the body. Another group of 
poisons of similar action are those produced within the body by 
putrefactive action or in various foodstuffs before ingestion. Fre- 
quently cases have been observed in which all the members of a 
family or even large numbers of people have been poisoned by 
eating certain meats, sausages, ice-cream, and other foods. In 
some of these cases it has been found that the toxic element was 
a basic compound resembling the alkaloids in chemical structure. 
To these putrefactive compounds the name ptomain is given. 
One of these compounds, which occurs in cheese, and occasion- 
ally in milk, has been termed tyrotoxicon. Intoxications of 
this class must be distinguished from infections resulting from 
the use of food contaminated with micro-organisms. The symp- 
toms may be so rapidly developed (absence of incubation period) 
and so immediately generalized that the distinction can be 
arrived at clinically, but the absolute diagnosis is made bac- 
teriological ly. 

A considerable number of ptomains have been separated, in- 
cluding neurin, obtained from putrid flesh ; muscarin and ethy- 
lendiamin, derived from decayed fish ; mydalein, and mydatoxin. 
Some of these substances produce toxic results indistinguishable 
clinically from those produced by certain alkaloids. This fact has 
become one of great importance in medicolegal investigations. 



THE ETIOLOGY OF DISEASE. 



31 



VEGETABLE AND ANIMAL PARASITES. 

Vegetable parasites are by far the most important causes 
of disease. The belief in a living cause or contagium vivum is by 
no means a recent acquisition, but the actual demonstration that 
diseases may be caused by minute living organisms has only 
recently been reached. The micro-organisms in question (bac- 
teria) belong for the most part to the vegetable kingdom and con- 
stitute the lowest orders of fungi. Their biologic characters and 
~their relations to special diseases will be described in a subsequent 
chapter. 

Etiologic Relationship of Bacteria to Disease. — It is difficult to 
prove the specific relation of bacteria to disease. Koch has laid 
down four important laws which must be conformed with before 
the etiologic importance of a bacterium is admitted. These are : 
(1) the bacterium must be found in the diseased person ; (2) it 
must be cultivatable upon media outside the body ; (3) pure 
cultures introduced into a healthy animal must produce the dis- 
ease in the animal ; and (4) the bacterium must be recoverable 
from the body of the animal. In a number of diseases micro- 
organisms have been proved to be the specific causes according to 
the requirements of Koch's rules. In other diseases it has not 
been possible to furnish absolute proof, though the presump- 
tive evidence, furnished by constant occurrence of the bacteria, 
suggestive association with the lesions of the disease, absence of 
the bacteria in other diseases, etc., is sufficient to satisfy all but the 
most sceptical. 

Classification of Diseases due to Bacteria. — The general term 
infectious disease is applied to all such as are caused by bacteria, 
In some cases the diseases are readily communicated from person 
to person, even though contact has not been immediate. These 
are termed contagious diseases, while the term noncontagious is 
given to those in which such ready transference is not observed. 
As a matter of fact, the distinction is artificial. Any infectious 
disease may be communicated from the diseased to the healthy if 
the germs or bacteria are transferred. In some diseases this trans- 
ference readily occurs, even through the air and at considerable 
distances ; in others actual contact is necessary ; while in still 
others secretions or excretions of the diseased must be conveyed 
to the healthy. Contagiousness is therefore a matter of degree 
only. 

Infectious diseases may at times spread in communities, affect- 
ing large numbers of people. Such a dissemination is termed 
epidemic, and the disease an epidemic disease. When the disease 
spreads over large areas, as a whole country or continent, the term 
pandemic disease is applied. Other infections are constantly 
present in a locality ; for such the terms endemic and endemic 



32 



TEXT-BOOK OF PATHOLOGY. 



disease are used. Some endemic diseases are restricted to certain 
localities and seem in some measure dependent upon local con- 
ditions (of atmosphere, soil, etc.) for their continuance. These 
are called miasmatic diseases. 

Infectious diseases are frequently described as local or general. 
Local infections are those that present specific pathologic change 
in a restricted part of the body ; the general organism suffers more 
or less in consequence. Examples of this are erysipelas and diph- 
theria. General infections are marked by an immediately gen- 
eralized disease, as in typhus fever or plague. Strictly speaking, 
most if not all of the so-called general infections are at first local. 
Among purely local infections might be named the diseases of the 
skin due to vegetable micro-organisms. 

Entrance of Micro-organisms into the Body. — Bacteria may be 
inhaled or swallowed, may enter through abrasions in the mucous 
membranes or skin, and may be transferred in utero from the 
maternal to the fetal blood. The mode of entrance in individual 
diseases depends upon the nature of the bacterium, its habitat, and 
surrounding conditions. Some may enter in but one way ; others 
gain access in any of the different ways. Details regarding this 
subject will be given in the discussion of special infections. 

Animal parasites of various kinds act as causes of disease. 
This group of diseases is termed the parasitic diseases or invasion 
diseases. In some instances the clinical course is similar to that 
of infectious diseases (malaria, dysentery, trichinosis) ; in other 
cases the manifestations bear little resemblance to infections. 



CHAPTER II. 

DISORDERS OF NUTRITION AND METABOLISM. 

Pood. — In the life of the organism certain substances are 
needed for the repair of tissues consumed in the wear and tear of 
life and to supply heat and other energy. Among these foods are 
proteids, carbohydrates, fats, inorganic salts, and water. A con- 
tinuance of normal existence requires more or less definite propor- 
tions of the first three and at least a sufficiency of salts and water. 
The amount of food and the exact proportions vary somewhat in 
individual cases and under varying circumstances. Voit found 
that a laboring man under ordinary conditions requires 118 g. of 
proteid, 56 g. of fats, and 500 g. of carbohydrates. The proteids 
of the diet are necessary to restore tissue-waste, since the organ- 
ism cannot build up proteids from simpler compounds. This con- 
sumes part of the nitrogenous foodstuffs. The rest, with most of 



DISORDERS OF NUTRITION AND METABOLISM. 33 



the fats and carbohydrates, is mainly useful in contributing 
energy. 

Diminished Supply of Food ; Inanition ; Starvation. — 

Either the want of food or disorder of the gastro-intestinal tract 
may lead to insufficient nourishment. This causes a loss of body 
weight, as the necessary heat-producing and energy-giving sub- 
stances must be supplied to maintain life, and the tissues are con- 
sumed for this purpose. The carbohydrates (glycogen of liver and 
muscles) and fats suffer first and most profoundly, and unimportant 
parts are reduced before the vital structures are attacked. The 
subcutaneous and other adipose tissues and the muscles first waste, 
then the liver, bones, heart, etc. 

The functions of various organs suffer greatly : the respirations 
and heart-action are weak, muscular exertions are reduced to a 
minimum, the endurance and nervous force decline, the body- 
temperature sinks, and finally death may occur from exhaustion or 
secondary affections consequent upon the disturbed nutrition (see 
Acid-intoxication). The blood in starvation preserves its corpus- 
cular richness surprisingly, even after prolonged abstinence. This 
is doubtless due to loss or evaporation of liquid ; the actual num- 
ber of corpuscles probably suffers reduction. 

Increased Supply of Food ; Overfeeding. — The effect 
of this depends upon individual conditions, such as the amount of 
exercise, the surrounding temperature, and less easily demonstrable 
peculiarities of the individual. An excess of proteid food leads to 
increased excretion of the end-product of its metabolism — urea. 
A very small proportion may contribute to building up a reserve 
amount of albuminous tissue ; this has not been positively proved. 
Great excess of proteid eventually disturbs digestion and leads to 
its discharge with the feces. 

The carbohydrates and fats are broken up in the body and ex- 
creted mainly as carbonic acid and water. An excess of these 
foods tends to cause increased deposition of reserve fat and glv- 
cogen, which may be called upon at subsequent times of need. 
This deposition is a normal or physiologic process and has the 
distinct purpose just indicated. Exceptionally in the condition 
called obesity the storing up of fat is inordinate and probably 
pathologic. 

Obesity. — The origin of fat is still a subject of controversy 
among physiologists. According to the oldest view, which, how- 
ever, is still adhered to by some, and has indeed been stronglv 
defended, the fat of the body is derived from that of the food, and 
the possibility of this has actually been demonstrated. Under 
ordinary circumstances, however, but little of the fat is so produced. 
Another school of physiologists maintained that the proteids of the 
food break up into a nitrogenous and a non-nitrogenous part, the 
former being finally excreted as urea and other substances or repair- 

3 



34 



TEXT-BOOK OF PATHOLOGY. 



ing the tissue- waste, the latter part contributing energy or forming 
fat. At the present time it must be admitted that though proteids 
may possibly form fat in this manner, the actual demonstration is 
still wanting. The main source of fat is certainly the carbohy- 
drates of the food. 

Causes of Obesity. — Excessive ingestion of food by persons 
having active digestion and leading sedentary lives may occasion 
unusual deposition of fat. It is difficult, however, to determine 
the limits between physiologic and pathologic fatness. In some 
cases patients assert that the amount of food has not been exces- 
sive, and this may be actually true. Obesity in such individuals 
is undoubtedly pathologic and clue to some inherent abnormality 
of metabolism. A further proof of the existence of such a ten- 
dency is seen in certain families, in which excessive fatness is 
common, even in childhood. The nature of this metabolic dis- 
order is obscure. It has often been held that the power of oxida- 
tion is lacking, and, as a matter of course, the amount of oxygen 
consumed is deficient in comparison with the amount of food in- 
gested. This must be true, or the fat could not accumulate ; but 
it remains to be shown whether the diminished oxygen-consump- 
tion is the primary cause or only an incident in the disease. 

Pathologic Anatomy. — The excessive adipose tissue in this 
disease is found in the skin and subcutaneous tissues, in the omen- 
tum and peritoneum, around the kidneys, heart, and mediastinal 
tissues, in the liver, and less commonly elsewhere. The amount 
varies from slight excess to monstrous deposits. Secondary changes 
in the organs (notably the heart-muscle) may be due to pressure 
or functional inactivity. 

Associated Conditions. — Fatness is more or less closely re- 
lated to certain other diseases of metabolism, such as diabetes and 
gout. Anemia is frequently present and has sometimes been re- 
garded as a cause, operating by reducing oxidation. (Further 
discussion of this subject is included under Fatty Infiltration.) 

Excessive Tissue-destruction. — This has been referred to 
in connection with inanition ; but it may occur as a condition in- 
dependent of the amount of food ingested. Among the conditions 
in which this is observed may be mentioned fever, infectious or of 
other forms ; chronic infectious diseases, with or without fever ; 
tumors, especially carcinoma ; intoxications of various sorts ; some 
cases of Graves' disease, etc. In all of these conditions the fats 
of the body may waste as in simple inanition ; but there is an early 
and marked tendency to consumption of the more important pro- 
teid structures. This latter consumption may proceed along 
physiologic lines, or there may be distinctly pathologic modifica- 
tions sometimes leading to serious results (see Acid-intoxication). 

The nature of the metabolic disturbances in these cases is ob- 
scure, though it is likely that toxic substances of various sorts are 



DISORDERS OF NUTRITION AND METABOLISM.- 35 



the direct causes. This is most probable in the case of direct in- 
toxications (phosphorus), but is also likely in other cases. In 
Graves' disease and carcinoma, as well as in fevers, there are 
doubtless poisonous substances in the blood, but whether these are 
the causes of the metabolic changes or not requires further study. 
The fact that thyroid extract is capable of causing excessive de- 
struction of tissue in normal or obese persons is significant in this 
connection. 

Acid-intoxication. — In the final metabolic transformation 
of proteids there are produced ammonium, urea, kreatinin, and 
other nitrogenous substances. The formation of urea is still 
obscure in some particulars. It is certain that a large part is 
produced in the liver, and it is probable that some is formed in 
the muscles. The intermediate steps in the manufacture of urea 
have not been definitely determined, but it is known that the liver 
is capable of converting ammonium salts clirectly into urea, and it 
is probable that ammonium is an important intermediate product 
of proteid transformation. An excess of acids in the body (either 
from introduction from without or production in the body) is in 
part neutralized by alkaline bases in the blood and tissue-juices, 
and in part by ammonium. In consequence of this consumption 
of ammonium the urea of the urine decreases and the ammonium 
salts are increased. The quantity of such salts is therefore in a 
measure an indication of the condition which has been termed 
acid-intoxication. The partial neutralization of acids by the fixed 
alkalies of the body causes reduced alkalinity of the blood and 
juices of the body. 

Experimental acid-intoxication is easily produced in animals by 
feeding them with foods deprived of alkaline bases, or by direct 
administration of acid. In the former case the acids (sulphuric 
from the sulphur of albuminous food ; and phosphoric from the 
phosphorus) resulting from transformation of food and tissues must 
be neutralized by the alkalies of the body and the ammonium pro- 
duced in the process of urea-formation in the liver ; in the latter 
case there is direct excess of acid. Such acid-intoxication is readily 
produced in herbivorous animals, as the amount of proteid food 
is small, and in consequence but little ammonium is produced. 
Various nervous symptoms are observed. The animal breathes 
quickly, the pulse grows rapid, muscular weakness, ataxia, and 
tremor develop, and finally coma or collapse terminates the dis- 
ease. The administration of alkalies may completely arrest the 
progress of the condition, and full restoration may occur. 

Acid-intoxication in Man. — Somewhat similar symptoms are 
seen in man in certain diseases in which decreased alkalinity of 
the blood and increased elimination of ammonium, with decrease 
of urea and the excretion in the urine of certain organic acids, have 
been discovered. The assumption is warranted that these are 
cases of acid-intoxication. 



36 



TEXT-BOOK OF PATHOLOGY. 



Etiology. — Among the diseases in which this occurs are fever, 
diabetes, carcinoma, acute yellow atrophy of the liver, severe 
anemia, phosphorus-poisoning, advanced gastro-intestinal disease, 
and inanition. Sometimes no discoverable cause can be detected 
(cryptogenetic acid-intoxication). Gastro-intestinal disorders are 
very likely the occasion of this form of obscure acidosis. Poisons 
produced in the intestines probably set in play the metabolic dis- 
turbances which terminate in over-production of acids. 

Among these acids are lactic, sarcolactic, sulphuric, phosphoric, 
diacetic, and /9-oxybutyric acid. These in part combine with the 
fixed alkalies and with ammonium, and in part are excreted as 
such. Some, as sarcolactic acid, usually suffer decomposition in 
the body, and are therefore rarely met with in the urine. 

The origin of the acids of the fatty acid series has been the 
subject of much controversy. Undoubtedly they may be derived 
from the non-nitrogenous part of proteids, and in most of the 
diseases above enumerated this is probably the case ; but they may 
be formed from carbohydrates as well. The increase of diacetic 
and /3-oxybutyric acids in cases of diabetes when small amounts 
of carbohydrates are supplied, and their decrease when the carbo- 
hydrates are increased, point to the fact that destructive consump- 
tion of proteids is the important source, though it may not be the 
only or invariable source. 

There is always reduction of oxidation in casts of acid-intoxi- 
cation, but it is not known whether this is the primary disturb- 
ance, or whether it is but an accompaniment. Experimentally it 
has been shown by several observers that diminution in the supply 
of oxygen will lead to increase of these acicls. They probably owe 
their presence to excessive production and to the failure of the 
normal oxidation which would reduce such bodies to simple ex- 
cretory products. Other substances may result from the same 
tissue-destruction with insufficient oxidation. Among these are 
the amido-bodies, lencin and tyrosin, found in the urine in phos- 
phorus-poisoning and acute yellow atrophy of the liver as well as 
in other conditions. 

Symptoms. — The symptoms of acid-intoxication in man may 
be quite similar to those seen in experiments upon animals. 
Marked dyspnea (air-hunger), rapidity of the pulse, depression, 
stupor, and deep coma (coma carcinomatosum, diabeticum) are 
some of the more pronounced manifestations. The production of 
these may be direct or indirect. The cause of these symptoms is 
very probably the acid-intoxication due to the presence of /9-oxy- 
butyric acid. Diacetic acid and acetone are derivatives of ./9-oxy- 
butyric acid. Aside from such direct action, acid-intoxication may 
effect its results by lessening the alkalinity of the blood and ab- 
stracting fixed alkalies from the fluids of the body. 

Formation of Albumoses. — In disturbed conditions of 
metabolism albumoses, or probably very rarely peptone, are formed. 



DISORDERS OF NUTRITION AND METABOLISM. 37 



The causes which t lead to the presence of these substances in 
the blood and their excretion in the urine are numerous. Fever 
of all kinds may be attended by this condition, and it may occur 
in the course of suppurations, or other forms of tissue-destruction 
(acute yellow atrophy, phosphorus-poisoning). It is found in 
ulceration of the gastro-intestinal tract, and in some cases of new- 
growths. The occurrence of albumosuria in osteomalacia has long 
been recognized. 

In all cases there is rapid tissue-destruction in which the albu- 
mins become hydrated, forming some variety or varieties of albu- 
moses, and possibly in rare cases peptone. Formerly the term 
peptonuria was generally used to designate what is now called albu- 
mosuria. The presence of albumoses in the blood causes no well 
recognized results. It is known that they retard coagulability, 
and their ingestion often causes leukocytosis. It is very likely 
that they have other effects, but these are obscure. 

The term peptone is now quite generally limited to the final hydration 
product according to the definition of Kiihne. The peptone of Briicke 
includes certain bodies now recognized as albumoses. 

Alloxin Bases and Uric Acid. — The investigations of 
recent years have shown that these substances are derived from 
the nuclein of cellular nuclei. The xanthin bases — xanthin, 
guanin, adenin,and hypoxanthin — are intermediary products which 
partially or largely become oxidized to uric acid. Normally the 
amount of uric acid is far in excess of that of the bases. Some of 
the uric acid may become further oxidized, with formation of urea. 
The great source of these products is cellular destruction, and 
especially that of the leukocytes. Abnormally large quantities are 
found in the urine in leukemia and in some cases of leukocytosis ; 
and in a measure the substances furnish an indication of leukocytic 
destruction. The kind of diet may influence the amount of these 
bodies, according as it is rich or poor in cellular tissue. The 
attempt to establish a relationship between certain disorders (head- 
aches, migraine, etc.) and increased production of alloxin bases has 
not as yet proved satisfactory. 

A theory of the etiology of gout has been proposed by Kolisch, in which 
it is held that the kidneys are mainly concerned in the transformation of 
the xanthin-bases into uric acid, and "that this function of the kidneys is re- 
duced in gout. The excess of xanthin-bases resulting from this cause in 
turn acts destructively upon the kidney-substance, which then fails to excrete 
the uric acid existing in the blood. This theory was based upon work per- 
formed with a faulty chemical method, and has therefore been discredited. 

A disease in some way dependent upon or associated with ab- 
normal formation of uric acid and alloxin bases is gout. 

Gout. — In its typical form gout is a paroxysmal disease 
marked by deposits of urates in the joints and other structures, 
and by coincident or consequent inflammatory disturbances. There 
are many varieties, however, of irregular gout in which the par- 



38 



TEXT-BOOK OF PATHOLOGY. 



oxysnis may be partly or wholly wanting and in which the disease 
takes the form of a general systemic disorder, or of organic mala- 
dies of various sorts. 

Etiology. — Gout is essentially a hereditary affection, the heredity 
not rarely being polymorphous. By this is meant that in certain 
families gout and other diseases, such as obesity, diabetes, and 
arterial sclerosis, may occur interchangeably. Gout usually de- 
velops in the later years of life, and among the contributing causes 
are the use of alcohol, overeating, sedentary life, and chronic lead- 
poisoning. 

Pathologic Anatomy. — The conspicuous anatomic lesions are 
those of the joints, and consist of the deposit of urate of sodium 
in the cartilages and connective tissue, and secondary inflammatory 
changes. The latter may cause great distortion and fibrous over- 
growth. Similar urate deposits may occur in the cartilages of the 
ear, eye, and nose, and in the subcutaneous connective tissue or 
elsewhere. These deposits, called the gouty tophi, may subse- 
quently disappear by absorption or by discharging through the 
skin. Cirrhosis in various organs and tissues of the body fre- 
quently occurs in the course of gout. Among these the cirrhotic 
or gouty kidney is most important. Atheroma, cirrhosis of the 
liver, hypertrophy and fibroid change in the heart, and chronic 
valvular disease are also frequent. 

Pathogenesis. — According to the older theory of gout, the dis- 
ease is due to increased quantities of uric acid in the blood. It 
has been found, however, that in other conditions — as, for example, 
lukemia — excess of uric acid may occur in the blood without any 
symptoms like those of gout, The uric-acid excretion of the urine 
has been found to decrease markedly during a few days before an 
attack, and the assumption has been made that the acid accumu- 
lates in the blood and is then deposited in the tissues. It is pos- 
sible, however, that changes in diet and the occurrence of the 
deposits themselves may be the cause of the preliminary fall in 
uric-acid excretion. Subsequently during the gouty attack the 
average excretion of uric acid does not differ from that seen in 
health. Prior to the deposits local cellular necroses are believed 
by many to be necessary for the deposit, and these necroses have 
been attributed to the excessive amount of acid. Proof is wanting, 
however, to show that excessive quantities of uric acid are capable 
of causing such degenerations or necrosis. In some cases trauma- 
tism may play a part in localizing the gouty precipitations ; in 
most cases, however, the cause is obscure. 

The cause of the fluctuation in the excretion of uric acid is 
still obscure. An old theory that diminished oxidation in the 
tissues is the immediate cause is no longer tenable ; and a newer 
view, which asserts that an accumulation of uric acid results from 
failure of the renal function, has not been established. 



DISORDERS OF NUTRITION AND METABOLISM. 



39 



Glycosuria and Diabetes. — A certain amount of grape 
sugar occurs in the blood and urine of normal persons. The 
quantity in the blood varies from 0.1 to 0.2 per cent. Notable 
increase above these figures constitutes a pathologic condition, 
hyperglycemia. Sometimes other forms of sugar, as levulose, occur 
in the blood and urine. When there is sufficient sugar in the 
urine to be discoverable by the ordinary tests, the condition is 
pathologic and is termed glycosuria. This may be transient and 
trivial in character, or a manifestation of a definite diseased con- 
dition called diabetes. 

The disposition made of carbohydrates by the animal body is 
not definitely known in all particulars. It is certain, however, 
that these substances are deposited in the liver and in the muscles 
in the form of glycogen, that they form fats, and are in part con- 
sumed by oxidation. The deposit of glycogen is of the nature of 
a reserve store, the system thus being prepared for intervals of 
abstinence. The glycogen is gradually discharged from these 
tissues, and thus the quantity of sugar in the blood is maintained 
at a more or less constant level. 

Alimentary glycosuria is a term applied to glycosuria occurring 
in healthy or diseased persons as a result of excess of carbohydrate 
food. It is easily produced by the administration of considerable 
quantities of milk-sugar, levulose, cane-sugar, or glucose. The 
drinking of beer seems to aid particularly in its development. 
The explanation of this condition seems a simple one. The 
organism is unable to store up or consume the amount of carbo- 
hydrates administered, and the excess is therefore discharged 
through the kidneys. The ease with which such glycosuria is 
developed differs in different individuals, and researches have been 
made to determine the conditions that favor its development. The 
liver in particular has been suspected as the organ most likely 
inefficient in these cases, but thus far no definite facts have 
been learned ; and the role of this organ has probably been exag- 
gerated. 

It is worthy of attention that alimentary glycosuria may occur in diabetes 
mellitus. The existing glycosuria is greatly increased, or, if the disease is 
not in an active stage, glucose may appear when excess of sugar or starch is 
administered, though it had not been present before. 

Experimental glycosuria, produced by administration of phlorid- 
zin, offers several puzzling facts for consideration. It shows that 
excess of glucose in the blood (hyperglycemia) is not a necessary 
condition for the occurrence of glycosuria. After administration 
of phloridzin, a glucoside which contains about 40 per cent, of 
sugar, there is no excess of sugar in the blood, but glucose appears 
in the urine, and indeed more than could have been produced by 
the entire quantity of phloridzin administered. This shows that 
there \s abstraction of sugar from the reserve stores in the body. 



40 



TEXT-BOOK OF PATHOLOGY. 



It is not unlikely that the renal cells play a part in the occurrence 
of this unusual excretion ; and this fact, together with the dis- 
appearance of sugar from the urine in the late stages of some cases 
of diabetes, when renal disease has occurred, has suggested to some 
the possibility of renal forms of glycosuria and diabetes. This 
view, however, has not yet been established. 

Clinical Causes of Glycosuria. — Glucose appears in the urine in 
many conditions, including dietary excesses, various infectious dis- 
eases, intoxications, and concussion, injury, or disease of the central 
nervous system, especially the floor of the fourth ventricle. 

Diabetes is a disease in which polyuria and glycosuria are 
marked symptoms. It is not improbable that the term includes 
disorders of quite different sorts, but no differentiation of such is 
possible at the present time. A mild and a severe form are dis- 
tinguished, and these present some striking differences, to which 
reference will be made below. 

Etiology. — Diabetes is frequently a hereditary disease, occurring 
in families in which the same disease or obesity and gout have 
occurred. The Jews seem particularly liable to it. Overeating, 
sedentary life, and gout are causes of some importance, especially of 
the milder form. Sometimes abnormal conditions of the nervous 
system may be the underlying cause. Among these are functional 
depressions, as in cases of excessive grief ; traumatic injuries with 
concussion of the brain ; and local diseases at the base of the brain 
in the vicinity of the medulla. In some cases disease of the pan- 
creas is the probable cause. Diabetes may occur in the young or 
after middle life, the milder cases more frequently occurring at the 
latter period. 

Pathogenesis. — In the milder cases of diabetes the same ex- 
planation may be applicable as that given for glycosuria, viz., the 
liver and muscles do not store up the carbohydrates carried to 
them, and the excess of sugar is not burned up in the tissues. 
Hyperglycemia with consequent glycosuria results. In these cases 
the withdrawal of carbohydrate food or temporary abstinence from 
all food may cause disappearance of the glycosuria. In severe 
cases this explanation is not applicable, since the amount of glucose 
in the urine is often but little affected by abstinence from carbo- 
hydrate food or even by starvation. It is quite certain that in 
these severe cases the tissues, especially the muscles, furnish the 
sugar excreted in the urine. In normal individuals, and even in 
those suffering with mild diabetes, the sugar thus liberated is burned 
in the tissues. Glycosuria does not therefore occur. Severe and 
mild diabetes differ only in degree : in one case the power to con- 
sume sugars is greatly deficient, in the other only moderately so. 

The nature of the metabolic disturbances that lead to this 
inability to dispose of carbohydrates is still very obscure. The 
old theory, that there is a lack of oxidizing power, is disposed of 



DISORDERS OF NUTRITION AND METABOLISM. 41 



t>y the experimental demonstration that oxidation may be nor- 
mally active. The influence of the nervous system is undoubted. 
Reference may here be made to the occurrence of diabetes after 
puncture of certain parts of the brain (medulla). At one time 
this was thought to act through the vasomotor mechanism, con- 
gestion and disturbance of function of the liver being regarded 
as the important consequence of vasomotor derangement. At the 
present time the part played by the liver is considered less im- 
portant. No satisfactory explanation of the role of the nervous 
system in the etiology of diabetes has been presented. 

Older pathologic studies showed that diseases of the pancreas 
are frequently associated with diabetes ; and recent experimental 
investigations emphasize this relationship. Removal of the pan- 
creas in the lower animals causes diabetes. It has not, however, 
been shown in what way pancreatic disease or ablation acts, though 
Lepine and others believe that the pancreas elaborates a glucose- 
destroying (glycolytic) ferment, whose absence under the conditions 
named causes accumulation of sugars in the blood and consequent 
glycosuria. Unfortunately, this view is not confirmed by the ex- 
periments of others ; and the theory is certainly not applicable to 
all forms of the disease, since diabetes may occur without discover- 
able disease of the pancreas. 

Metabolism in Diabetes. — The essential fact is the inability of 
the body to consume carbohydrates for the production of energy. 
As long as excess of proteid and fatty food is taken and consumed, 
no disturbance of the general metabolism results ; but when diges- 
tion fails or the diet is poorly regulated, destruction of the proteids 
of the body with increased excretion of urea occurs. Emaciation 
may be prevented for a time by increased consumption of proteid 
food, but eventually occurs. In the destruction of the proteids 
of the food and tissues, acids are formed in excess (phosphoric from 
the phosphorus, sulphuric from the sulphur, /?-oxybutyric and 
diacetic from the non-nitrogenous part of the albumins), and the 
condition termed acid-intoxication (see above) results. A conse- 
quence, and to some extent a measure, of this is the increased ex- 
cretion of ammonium salts in the urine. The uric acid of the urine 
is but little increased in diabetes. 

Pathologic Anatomy. — Aside from the lesions already referred 
to as in some way related to the causation of the disease, there are 
found pathologic changes of various kinds that result from it. 
The lesions of gout (arteriosclerosis and cirrhotic kidneys) may be 
of the nature of mere concomitants, or may be direct results of 
diabetes. Renal diseases are of peculiar interest. Late in diabetes 
albuminuria frequently develops and interstitial nephritis may fol- 
low. When this occurs the glycosuria and other symptoms of 
diabetes sometimes subside. The explanation of this is obscure 
(see under Glycosuria). Changes in the liver (cirrhosis) have 



42 



TEXT-BOOK OF PATHOLOGY. 



often been found, and have been regarded as causative in some 
cases. A peculiar form of diabetes with hepatic disease and 
general icteroid staining (hemochromatosis) of the skin and other 
tissues has been described under the title diabete bronze. Skin 
eruptions (eczema, furuncles, carbuncles) are frequent in certain 
forms of diabetes, and gangrene of the extremities is common. 
Pneumonia and pulmonary tuberculosis are among the frequent 
developments of late stages of the disease. Chronic endocarditis, 
neuritis, and cataract are comparatively rare lesions. The blood 
in diabetes is less alkaline than normal and contains an excess of 
solid matter, particularly when great polyuria has led to inspis- 
sation. 

Oxaluria. — This term is, strictly speaking, applicable only to increase of 
oxalic acid in the urine, but is usually employed for cases in which crystals 
of oxalate of lime are found abundant in the urine. The normal maximum 
of oxalic acid is 20 mgr. for twenty-four hours. It has been sometimes held 
that oxaluria is a result of deficient oxidation of the carbohydrates or of 
the albumins of the body, but this theory has not been established. True 
oxaluria determined by chemical estimation of the total excretion of oxalic 
acid has been found in jaundice and in some cases of diabetes. The authors 
who have argued in favor of a specific disease marked by nervous symptoms 
and oxaluria based their observations on the presence of an excess of oxa- 
late sediment, rather than on chemical examinations. Increased sediment 
occurs in certain instances of gout in which the oxalates alternate with uric 
acid or coexist with this. In these cases, as in cases of oxalate calculus in 
the kidney or bladder, the important causative factor is most probably some 
alteration in the constitution of the urine, such as conversion of monosodic 
phosphate into the disodic phosphate, that reduces the solvent power of 
the urine for oxalate of lime. 

Phosphaturia. — This term should be restricted to increased excretion 
of phosphoric acid, rather than to the presence of increased phosphate sedi- 
ment in the urine. The latter may be due simply to want of acidity of the 
urine. The daily maximum of phosphoric acid with ordinary diet is from 
3.5 to 4 g. The term phosphaturia might also be applied to cases in which 
no absolute excess of phosphoric acid is found, but in which this substance 
is relatively in excess when compared with the excretion of nitrogen. The 
normal proportions are from 17 to 20 parts of phosphoric acid for 100 parts 
of nitrogen. Phosphaturia in the sense just described has been found in 
some cases of inanition. Decided increase in the phosphatic excretion, ab- 
solute as well as relative, occurs in some cases of diabetes ; also in cases of 
tuberculosis and disease of the bones, such as ostitis and osteomyelitis. In 
considering the question of phosphatic excretion in the urine it is important 
to remember that the greatest portion of phosphoric acid is derived from, 
the food, only minor quantities coming from the metabolic consumption of 
tissues. Further, it must be remembered that much of the phosphoric acid 
of metabolism is excreted through the bowel. The term diabetes phosphatide 
has been used by Teissier for phosphaturia in the sense of increased total 
excretion, and four varieties have been described : (a) cases with polyuria 
and marked nervous symptoms; (b) cases preceding or accompanying pul- 
monary diseases, especially tuberculosis; (c) cases in which phosphaturia 
alternates with or coexists with glycosuria ; and (d) cases in which oxaluria, 
polyuria, and slight albuminuria are present and in which there is some re- 
lationship with gout. 

The nature of the metabolic disturbances in phosphaturia are obscure. 
Sometimes the disorder of metabolism seems to be merely quantitative, in 
other cases doubtless qualitative. 



DISORDERS OF NUTRITION AND METABOLISM. 



43 



FEVER. 

Definition. — It is not easy to define this term accurately, 
though we may regard as fever a condition in which the tempera- 
ture of the body is elevated above the normal (98.6° F. ; 37° C.) 
and in which the tissue-metabolism is altered in the direction of 
increased consumption. There are cases in which the latter is in- 
significant or wanting, and there are other instances in which the 
temperature remains normal or subnormal under influences that 
ordinarily provoke fever. It is doubtful whether mere elevation 
of temperature, such as occurs in experimental injury of certain 
parts of the brain, constitutes fever ; but unquestionably it would 
be improper to apply this term to conditions of excessive tissue- 
destruction without elevation of temperature. 

Nature. — It is important, first, to consider the regulation of 
the temperature in health. In the normal individual heat is pro- 
duced in the body by constant oxidation and other metabolic 
activities, and the excess is dissipated by radiation from the sur- 
face and the heating or evaporation of excreta. These processes 
of heat-production and heat-dissipation are regulated in an orderly 
manner under the influence of the nervous system. Special centers 
for the production, dissipation, and regulation of heat have been 
described by the physiologists, though their location and method 
of operation still remain in doubt. Whatever the exact mechanism 
may be found to be, it is quite certain that in some way the ner- 
vous system exercises a control over production and discharge of 
heat. 

The excessive heat of fever may conceivably be due to excess 
of heat-production, to diminution of the dissipation, to both of these 
conditions, or to increase of both with greater excess of produc- 
tion. In most instances of fever in man it appears that produc- 
tion and dissipation are both increased, though the latter is in- 
sufficient. At the onset heat-dissipation may for a time be 
diminished. The increased production results from increased 
oxidation and other metabolic processes. A study of the respira- 
tory exchange of gases shows that oxygen is consumed in greater 
quantity than normally, and the quantity of C0 2 is correspond- 
ingly increased. The excess may amount to as much as 20 per 
cent., but in part this increased oxidation is due to the stimulation 
of muscular contractions in rigor, etc. Investigation of the ex- 
creta shows at the same time evidences of more or less rapid and 
extensive tissue-waste. The quantity of nitrogen eliminated is in 
excess of that consumed in the food, and wasting of the tissues 
results. The albuminous elements suffer particularly in the meta- 
bolic wasting, the decrease of fat being more especially dependent 
on insufficiency of food. 

Etiology. — The causes of fever doubtless vary greatly. Di- 



44 



TEXT-BOOK OF PATHOLOGY. 



rect exposure to heat does not affect the temperature more than a 
fraction of a degree in healthy persons, unless the surrounding 
temperature is very great. Ordinarily the heat-regulating mech- 
anism maintains a proper adjustment. Excessive heat may, how- 
ever, bring on fever, as in the case of sunstroke. Here, it has 
been held that the heat leads to direct disturbances of the nervous- 
regulating apparatus ; but recent investigations seem to show that 
there are first produced toxic substances which secondarily influ- 
ence the heat-centers of the brain. In another class of cases still 
more direct disturbance of heat-regulation seems to occasion fever. 
Among these cases are the instances of fever in hysteria and other 
nervous diseases. 

In the great majority of cases of fever it is quite certain that 
toxic substances are the cause of the febrile disturbances. These 
substances may be of quite different sorts. In the case of infections 
it is known that certain substances contained within the bacteria 
themselves may cause fever, and that products of the growth of the 
micro-organisms may have the same effect. The latter are prob- 
ably of albuminous nature. Other albuminous bodies resulting 
from normal or disturbed metabolism, independent of the action 
of bacteria, such as albumoses, peptone, tissue-fibrinogen, etc., may 
be equally potent ; and various ferments, such as pepsin, fibrin- 
ferment, diastase, etc., are known to have the same power. These 
facts explain the multiplicity of causes capable of producing fever, 
as any chemical, mechanical, or bacterial injury of the tissues may 
liberate toxic substances, which in turn act upon the nervous 
system and occasion the phenomena of fever. 

Pathologic Physiology. — Fever is accompanied by or leads 
to a variety of disorders. The appetite is lost, there is excessive 
» thirst, emaciation is habitual, and the functions of the various 
organs are more or less disturbed. To a large extent these results 
are doubtless due to the presence of toxic substances in the blood 
and to other changes in this fluid. There is always a tendency to 
inspissation of the blood, the number of corpuscles being augmented 
(relatively) and the specific gravity increasing. This is not, how- 
ever, invariably the case, as destruction of the solid matters of the 
blood may exceed the loss of liquid. The alkalinity of the blood 
is more or less reduced by the production of various acids in the 
increased tissue-destruction. A common or possibly characteristic 
metabolic process is the hydration of the albuminous tissues with 
formation of albumoses. There is little accurate knowledge of 
the toxic substances in the blood. The original poisons that 
caused the fever may be toxic for the entire organism, and other 
poisons may be produced by the elevation of temperature and 
the disturbed metabolism. 

Pathologic Anatomy. — Definite morbid changes may occur 
in the various tissues of the body, notably the muscles, heart, liver, 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 45 



and kidneys. Among these changes are cloudy swelling, fatty 
degeneration, and coagulation-necrosis. It is unlikely that these 
changes are the direct result of the increased temperature. More 
probably they result from the action of toxic substances generated 
in the course of the fever. 

Conservative Effects of Fever. — While fever occasions 
many disturbances and leads to various pathologic consequences, it 
is not improbable that there is a certain measure of usefulness in 
it. Some authors have called attention to the fact that rapid 
reduction of the temperature under the influence of antipyretics 
is often followed by harmful consequences. This does not neces- 
sarily prove the usefulness of the fever, as the antipyretics are all 
capable of harm in themselves. A more definite proof of the uses 
of fever is that obtained by subjecting infected animals to high tem- 
peratures or to febrile conditions, and then studying the progress 
of the infection. Under these circumstances it has been found 
that the course of various infections, such as with the Diplococcus 
pneumonia?, the bacillus of typhoid fever, and other organisms, is 
much milder and the consequences less serious than in animals not 
placed under the same conditions. These results agree very well 
with experiments with bacteria outside the animal body. For 
example, it is known that many of the bacteria are influenced 
unfavorably in their growth and virulence by excessive tempera- 
tures (104° to 107.6° F. ; 40° to 42° C). Whether in the body 
the temperature affects the micro-organisms directly or indirectly 
through the production of antitoxic substances, or in other ways, 
remains unsettled. It is not unlikely that increased circulation 
and respiration favor the elimination of the toxins that cause 
the fever. Increased toxicity of the urine has been found, but 
the methods employed are open to criticism. 



CHAPTER III. 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 

GENERAL DISTURBANCES. 

The circulation of the blood is maintained by the rhythmic 
contractions of the auricles and ventricles of the heart, aided by 
the elasticity of the arteries ; by the compression of the veins by 
the muscles; and by the suction of the inspiratory movements of 
the chest. 

General disturbances of the circulation result from lessened or 



46 



TEXT-BOOK OF PATHOLOGY. 



excessive heart-power, from arterial disturbances, or from changes 
in the quantity or character of the blood. Muscular and respira- 
tory weakness may be contributing causes. 

Weak Heart. — There are various forms of heart-disease that 
may lead to disordered circulation. The muscle itself may be 
weakened from overstrain, the fevers or other diseases, the action 
of poisons or insufficient nourishment, as in the anemias, or from 
narrowing of the coronary artery. The muscle may be soft and 
cloudy, fatty, or hardened by sclerotic changes. There may be 
no evident muscular disease, but merely functional weakness of 
the intracardiac ganglia. The valves or orifices of the heart may 
be diseased, and regurgitation or obstruction of the blood-flow re- 
sults. Sometimes blood-clots form within the heart and similarly 
cause obstruction of the current. Finally, pericardial effusions 
or adhesions or tumors pressing upon the heart may seriously dis- 
turb its action. 

The result of the weakened state of the heart must be the 
accumulation of blood in the venous system. The place of 
engorgement depends upon the part of the heart specially weak- 
ened. If the left ventricle fails, the blood backs into the left 
auricle and the lungs. As long as the right heart maintains its 
poAver the venous congestion goes no further ; but when this fails 
repletion of the right auricle and of the systemic veins ensues. 
When the right heart is first at fault general venous congestion 
is an earlier manifestation. In all cases the arterial pressure falls 
and the blood-current is slowed, whereas the venous pressure is 
increased. 

Sudden and complete failure of the heart causes anemia of the 
brain and syncope, which may prove fatal if not instantly relieved. 

Hypostatic Congestion. — In cases of serious weakness of the 
heart, in Avhich it is quite unable to maintain an active circulation, 
the blood tends by the force of gravity to sink to dependent parts. 
This condition is known as hypostatic congestion. It occurs very 
frequently in low fevers and quite commonly just before slow death 
resulting from any cause. Dilatation of the vessels from vaso- 
motor paresis, general muscular weakness, and the failure of 
vigorous inspiratory efforts are secondary causes. 

The blood accumulates in the skin of the back, especially about 
the buttocks. The skin is of a livid color, but is bloodless over 
the bony points ; the tissues tend to become sodden from transu- 
dation of liquid from the blood-vessels. Sloughing and gan- 
grene (bedsores) may result. Internally, hypostatic congestion 
affects the lungs particularly, and a form of pneumonia may 
follow. 

Post-mortem lividity is allied to hypostatic congestion. After 
death the blood gravitates to the dependent parts and accumulates 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 47 



especially in the veins, as the arteries contract as soon as the heart- 
action ceases. 

Overaction of the heart is less frequent than weakness. 
Temporary overaction occasions increased activity of the circu- 
lation and elevation of blood-pressure, sometimes sufficient to cause 
hemorrhage. More prolonged overaction due to overwork, to ex- 
cessive feeding, or to nervous stimulation, as in Graves's disease, 
causes hypertrophy of the left ventricle, and later of the whole 
organ. In consequence the circulation may be more or less per- 
manently overactive. 

Arterial Disorders. — Both organic and nervous disturbances 
are important. Of the organic disturbances the most frequent is 
sclerosis of the arteries, which offers a constant impediment to the 
arterial circulation. Hypertrophy of the heart overcomes the ob- 
stacle, but when the heart fails venous congestions and dropsy en- 
sue. Sclerosis may also affect the veins, but much less commonly. 
Local diseases of the aorta, as congenital narrowing, compression 
by enlarged glands or tumors, aneurysms, and blood-clots may 
obstruct the flow of blood to the arteries, and thereby cause stag- 
nation of the blood in the heart, lungs, and venous system. 

Vasomotor disturbances are dependent upon the nervous system. 
Under the influence of certain diseases of the nervous system or 
of poisons (as carbonic acid gas in asphyxia) acting locally on the 
vessels or upon the vasomotor center in the brain, contraction of 
the smaller arterioles occurs ; and in consequence the blood-press- 
ure is greatly elevated, the heart is impeded, and venous conges- 
tion results. On the other hand, the arterioles may distend from 
vasomotor paresis, the blood-pressure falls, and unless the heart is 
active there is a tendency to hypostatic congestion. 

Changes in the Blood. — Increase and decrease of the 
quantity of the blood are generally merely passing conditions to 
which the circulation readily adapts itself by dilatation or con- 
traction of the vessels. Sudden losses of blood, if large, may be 
fatal by syncope. Smaller losses are soon repaired by absorption 
of water from the tissues and by regeneration of blood. Increases 
in the quantity of the blood by ingestion of liquids never disturb 
the circulation greatly. Rapid excretion soon reduces the quantity 
to the normal. 

Changes in the character of the blood may affect its circu- 
lation. The accumulation of carbonic acid and probably other 
effete products of tissue-change impede the flow by exciting vaso- 
motor contraction. This is probably brought about by the action 
of the poisons on the terminal nerve-filaments in the blood-vessels 
or directly on the walls of the vessels. This is the best explana- 
tion of the increase of pressure in cases of Bright's disease without 
arteriosclerosis. The poisons in this case are the retained renal 
excreta. 



48 



TEXT-BOOK OF PATHOLOGY. 



LOCAL HYPEREMIA. 

Local hyperemia is increase in the quantity of blood in a part 
of the body. This may be due to increase of the flow to that part, 
or to obstruction of the outflow. The former is called active or 
arterial hyperemia or congestion ; the latter, passive or venous 
hyperemia. 

Active hyperemia occurs in organs during periods of func- 
tional activity, the increased blood-supply here being due to 
increased demand for nutrition. Pathologically, active hyperemia 
is due to causes which lead to dilatation of the arteries of a certain 
part. This dilatation may be due to influences acting through the 
vasomotor nervous system or to local affections of the vessel-walls. 
The vasomotor nervous system may be affected at its center in the 
medulla or peripherally. The latter is seen when the .sympathetic 
nerves, which contain vasoconstrictor libers, are severed or com- 
pressed by tumors, the vessel-walls thereby becoming paralyzed 
(neuroparalytic hyperemia). The superficial congestive hyperemia 
in fevers is probably due to the central vasomotor action of the 
toxic causes of fever. On the other hand, the vasodilator fibers 
in the spinal nerves may be stimulated, as in certain cases of 
neuritis, with a similar result [neurotonic hyperemia). Direct 
injury to the vessel- walls by heat, traumatism, inflammation, 
drugs, or by the vascular fatigue following temporary stoppage 
of the circulation, is a frequent cause. 

Active hyperemia is spoken of as collateral when anemia in one 
part leads to overfilling of the vessels of an adjoining or even 
distant part. 

The hyperemic area is bright red in color, the temperature is 
elevated, and there is slight swelling. After death the distended 
arteries and capillaries may contract and the part grows paler. 
Arterial hyperemia is one of the phenomena of beginning inflam- 
mation, and in any case if prolonged may terminate in inflam- 
mation. Functional activity is increased by moderate conges- 
tions. 

Passive hyperemia is clue to impediments to the outflow of 
the blood through the veins. This may be brought about by 
compression of veins by tumors, by thickening of their walls, or 
by thrombi within. Little disturbance results from obstruction 
of a small vein, because of the freedom of collateral circulation, 
provided the heart is active. In cases of weak heart-power, how- 
ever, slight obstructions may determine local venous hyperemia, 
or by gravity alone the blood may accumulate in dependent parts. 
The latter constitutes hypostatic congestion (see page 46). 

Areas the seat of passive hyperemia are dark red (cyanosis) and 
lowered in temperature. The veins are distended, and very soon 
the watery elements of the blood transude and the part becomes 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 49 



edematous and swollen. In severe cases red blood-corpuscles 
escape by diapedesis. 

This occurs in the small veins and capillaries, but not in the arteries. 
In consequence of the increased intravascular pressure the, red corpuscles 
are pushed through the wall of the vessel at the points of junction of adjacent 
endothelial cells. At these points the cement substance is found in greater 
abundance than along the borders of the cells, and the escape of the corpuscle 
takes place through the semi-solid cement substance. 

Later fatty degeneration results from the imperfect nutrition 
of the tissues ; or even necrosis and gangrene may occur. In 
long-continued moderate passive hy- 
peremia overgrowth of connective _ _ „.-^ : "^"> : . ^ 
tissue and pigmentation of the tissue , — . - ^| 
by broken-down blood-corpuscles is 
observed (brown induration). 

Complete stoppage of the circula- 
tion in a localized area is called stasis 
(Fig. 1). This may be an extreme 
grade of passive hyperemia. The 
blood-corpuscles accumulate in the 
small vessels (arteries, capillaries, 
and veins), and the plasma is slowly 
pressed through the vessel-wall or 
onward in the vessel. There results 
a filling of the vessel with a homo- 
geneous red material, which is com- 
posed of the red corpuscles so closely 
packed as to be indistinguishable. 
On relief of the stasis the corpuscles 
become free again. Stasis may also 
be produced by chemical agents 
which rapidly withdraw the plasma 
from the vessels, leaving the corpuscles unable to circulate ; or 
similarly by rapid evaporation of the liquor sanguinis from internal 
structures (as the peritoneum) exposed to the air. 

Passive congestion of any grade and stasis interfere with func- 
tional activity in two ways : by the reduction of nutrition of the 
cells and by the pressure exercised upon them by the accumulating 
blood and serum. 




Fig. 1.— Stasis of blood in the 
superficial vessels in a case of val- 
vular disease and heart-failure 
(modified from Ziegler). 



LOCAL ANEMIA. 

Local anemia or ischemia is the condition in which a tissue 
contains less than its proper quantity of blood. This may be 
direct when it results from causes obstructing the flow into the 
arteries, or collateral when it is due to withdrawal of blood into 
hyperemic areas in other parts of the body. Of the causes acting 

4 



50 



TEXT-BOOK OF PATHOLOGY. 



directly, pressure is the most frequent. There may be general 
pressure upon an organ or localized area of the body, as in the 
application of elastic bandages ; or pressure upon the vessels 
within the tissue itself, as in amyloid disease, the amyloid sub- 
stance compressing the arteries and capillaries, or there may be 
direct compression of an artery by tumors. The circulation in an 
artery may be impeded by sclerosis of the vessel-walls and by 
emboli or thrombi within the vessel. Local anemia of moderate 
or even severe grade may be due to nervous influences acting 
through the vasomotor system, as in the 
earlier manifestations of Raynaud's disease. 
Collateral anemia is well illustrated by the 
anemia of the brain occurring in animals 
in which the splanchnic nerves have been 
cut, with the consequent production of ab- 
dominal hyperemia. When ischemia is 
due to obstruction of a single vessel the 
circulation is generally soon restored by 
collateral anastomosis ; the collateral ves- 
sels sometimes reach considerable dimen- 
sions (Fig. 2). When an artery which has 
few anastomoses and which soon splits up 
into capillaries is obstructed the phenom- 
ena of infarction (see page 55) ensue. 

An anemic area is pale, reduced in size 
and temperature, and functionally less ac- 
tive than normal. If the condition per- 
sists, fatty degeneration and necrosis 
result. When a severe local anemia is 
relieved it is apt to be followed by hyperemia of the same area, 
due to exhaustion or degenerative weakness of the vessel- walls. 




Fig. 2.— Anastomoses three 
months after ligation of the 
femoral artery of a dog (Porta). 



HEMORRHAGE. 

By hemorrhage is meant the escape of the several con- 
stituents of the blood from the blood-vessels. It is said to be 
arterial, venous, or capillary according to the vessel from which 
the flow of blood takes place, and parenchymatous when it comes 
from all of the vessels. Hemorrhage may occur either by dia- 
pedesis and extravasation through intact vessels {hemorrhage per 
diapedesim) or by actual rupture of a vessel {hemorrhage per rhexin). 
The former process is seen only in the capillaries and smaller veins ; 
the latter occurs mainly in the arteries and veins. 

Diapedesis and Emigration. — Under normal conditions 
a certain number of white corpuscles by virtue of their ameboid 
movements escape from the capillaries, and become wandering 
cells which move about in the tissues or are carried by the lymph- 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 51 



stream. This process is called emigration. There is at the same 
time some transudation of plasma, which, with the leukocytes, 
enters the lymphatic circulation. Under certain abnormal condi- 
tions the red corpuscles also pass through the vessel-wall and col- 
lect in the tissues. This is known as diapedesis (Fig. 3). It may 
be studied very readily under the microscope in the mesentery of a 
living frog. It is noticed that the red corpuscles approach certain 
parts of the wall of the capillary or vein and become fixed ; then 
a small projection appears outside the vessel, opposite the corpus- 
cle, and as this increases the corpuscle within grows smaller, until 
the whole body has gradually passed through. Not rarely several 




Fig. 3.— Diapedesis of the red blood-corpuscles through a capillary of a frog's tongue 

(after Thoma). 

corpuscles pass through in one mass ; as has been particularly 
noted by Thoma. Outside the vessel the corpuscle at once as- 
sumes its ordinary shape. 

Diapedesis was first studied by Strieker and Cohnheim. Arnold,»whose 
investigations are most important, first believed that the emergence of the 
red corpuscles takes place through orifices or stomata ; but later recognized, 
as is now generally believed, that the supposed stomata are merely accumu- 
lations of intercellular substance in certain places between adjoining endo- 
thelial cells or at the junction of several cells. The active cause of the 
extrusion of the red corpuscles is the pressure of the blood. 

The leukocytes emigrate from the vessel in exactly the same 
way as the red corpuscles, but mainly by their own ameboid move- 
ments. At the same time there is a more or less copious outflow 
of plasma. 

Diapedesis is readily induced by mechanical compression of a 
vein, which elevates the blood-pressure ; or it may follow elevation 
of blood-pressure from any other cause. On the other hand, Avith 
normal pressure increased permeability of the vessel-walls may 
occasion diapedesis. Such degenerative conditions of the vessels 
may be due to the action of poisons, to various infectious diseases, 
to moderate traumatism, or to temporary obstruction to the flow 
of blood into a certain area. Perhaps also altered states of the 



52 



TEXT-BOOK OF PATHOLOGY. 



blood may play a part when both the vessels and pressure are 
normal. Hemorrhages by diapedesis are generally small and 
punctate (petechia?), but may be quite large, as sometimes in the 
conjunctiva. 

Causes of Hemorrhage. — The ordinary form of hemor- 
rhage per r hex in may be due to traumatism, to diseases of the 
vessels, to increase of the blood-pressure, and to certain vague 
nervous influences. 

1 . Traumatic hemorrhage may be due to direct laceration of a 
vessel or to contusions which merely weaken the vessel-wall and 
lead to subsequent rupture. 

2. Diseases of the blood-vessels causing hemorrhage generally 
originate from causes within the vessel, and are due to such con- 
ditions as poisoning, infectious fevers, cachexias, or the anemias. 
Among the diseases of the vessels are fatty degeneration of the 
intima or media, atheroma, and miliary aneurysm. On the other 
hand, the outer coat may be eroded by surrounding disease and 
hemorrhage ensue (hemorrhage per diabrosin). This is seen in 
phthisical cavities in the lungs. 

3. Increase of blood-pressure may be absolute or relative. The 
former occurs from emotional excitement, from hypertrophy of the 
heart, during paroxysms of whooping-cough, croup, and various 
convulsive disorders. In asphyxia there is decided increase of 
blood-pressure both from vasomotor contraction and from the 
violent muscular efforts. Relative increase of pressure occurs 
when the pressure external to the vessel is reduced, as in balloon 
ascension, or in the pleura in cases in which during violent in- 
spiratory efforts the air cannot enter the lungs, as in the fetus at- 
tempting to breathe during labor. 

4. Neuropathic Hemorrhage. — The nervous system exercises a 
peculiar influence upon the vessels. In cases of apoplexy, of 
epilepsy, and of section of the spinal cord, and in other nervous con- 
ditions, spontaneous hemorrhages from the nose or stomach, or into 
the lungs, suprarenal bodies, and other organs, are not infrequent. 
In the same group also are to be reckoned the instances of 
vicarious hemorrhage due to suppression of the menses, and the 
remarkable cases of stigmatization. The last named is a condition 
in which under nervous exaltation or hysteria spontaneous hemor- 
rhages occur from various parts of the body, especially from the 
parts wounded in the crucifixion. 

5. The Hemorrhagic Diathesis. — Certain persons present an in- 
herited tendency to bleed spontaneously or after very trivial injuries. 
Such persons are known as " bleeders,' 7 and the condition as hemo- 
philia. The exact pathologic condition which occasions the 
hemorrhages is still uncertain. A hemorrhagic diathesis may also 
be developed as a result of various diseases, as typhus fever, 
anthrax, septicemia, or phosphorus-poisoning. The same is ob- 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 53 



served in the severe forms of anemia, like progressive pernicious 
anemia and leukemia. In these eases altered blood states and 
disease of the vessel-walls are doubtless the causes at work. 

Classification of Hemorrhages. — Hemorrhage may occur 
on free surfaces or into the tissues. In the former case various 
names are applied to designate the locality, such as epistaxis, nose- 
bleed ; hemoptysis, hemorrhage from the lungs ; hematemesis, from 
the stomach ; enter or rhagia, from the bowel ; metrorrhagia, uterine 
hemorrhage between, and monorrhagia at, the menses. 

Hemorrhages into the tissues take their names from the size 
and nature of the lesion. A hemorrhagic infiltration beneath a 
surface, as of the skin or mucous membrane, is called an ecchymosis, 
which if small and well denned is a petechia, but if large and 
diffuse, a suggillation or suffusion. A distinct accumulation of 
blood, constituting a veritable blood-tumor, is known as a hema- 
toma. Infiltrations of a peculiar sort, involving localized portions 
of a tissue or organ, are known as hemorrhagic infarcts (q. v.). 

Results of Hemorrhage. — A very large hemorrhage may 
cause sudden death by cerebral anemia. More frequently the 
patient remains unconscious for a time and then slowly recovers. 
The hemorrhage ceases spontaneously by the diminution in heart- 
action, by clotting of the blood at the point of rupture, by retrac- 
tion of the elastic vessels, and by pressure of the surrounding 
tissues. Blood extravasated in the tissues soon coagulates and 
subsequently undergoes disorganization, the red corpuscles break- 
ing down into pigment-matter, which may be carried away or 
deposited at the seat of hemorrhage. The fluid elements may be 
completely absorbed, or, stained with coloring-matter, may remain 
as a cyst. A focus of hemorrhage may set up reactive inflam- 
mation and lead to encapsulation by new connective tissue. Some- 
times hemorrhagic accumulations become inspissated and undergo 
calcification. Blood in the serous sacs does not readily coagulate, 
but mingles with the normal liquid secretion. It may be grad- 
ually absorbed or may undergo degenerative changes, especially 
when infected by micro-organisms. Large hemorrhages cause acute 
anemia; repeated small extravasations may lead to profound sec- 
ondary anemia. (These conditions will be more fully discussed 
under Diseases of the Blood.) 

EMBOLISM. 

Embolism is the process in which foreign bodies of various 
kinds are carried in the blood and deposited in the smaller arteries 
or capillaries through which their size does not permit them to 
pass. The bodies deposited are called emboli. 

Sources and Nature of Emboli. — The most common form 
of embolism is that in which portions of thrombi situated in 



54 



TEXT-BOOK OF PATHOLOGY. 



the heart, the large veins of the extremities or pelvis, or on ather- 
omatous patches in the aorta, are swept into the circulation and 
lodge in the smaller vessels. Softening of the original thrombus 
is generally the immediate cause. More rarely portions of a dis- 
eased heart-valve or of the intima of the heart or arteries, liver 
or placental cells, or parts of tumors, are carried in the circulation 
and deposited as emboli. Disorganization of the blood may cause 
embolism of pigment-particles, as in malaria, or of small hyaline 
masses, as in burns and certain forms of poisoning. In cases of 
fracture of bones particles of fat may be dislodged from the mar- 
row and enter the circulation, while in wounds of the large veins 
of the neck or elsewhere air-embolism is observed. Finally, 
masses of bacteria, scolices of echinococcus, and other parasites 
are a serious form of emboli. 

Seats of Embolism. — The final place of lodgement of an 
embolus depends mainly on its source. Those derived from the 
general venous circulation are usually carried through the right 
heart to the lungs, where they occlude branches of the pulmonary 
artery. Emboli in the portal circulation may lodge in the liver, or 
pass through the liver to the heart and lungs. In cases of whooping- 
cough or other conditions attended with increased intrathoracic 
pressure emboli in the inferior vena cava may be carried in the 
direction opposite to the usual blood-current, and may be con- 
veyed into the liver through the hepatic veins. This is known 
as retrograde embolism. 

Emboli coming from the left heart or from the aorta are dis- 
tributed in the general arterial circulation. They are most fre- 
quently found in the spleen, kidneys, and brain. Other organs or 
the peripheral vessels may likewise be atfected, but the results of 
embolism are less marked in them and are frequently overlooked. 
Emboli from the veins may reach the general circulation in cases 
in which the foramen ovale or septum ventriculorum is perforated 
(paradoxic embolism), or by being broken up into smaller emboli 
in the lungs and thus passing through the pulmonary capillaries. 
The latter is not infrequent in cases of fat-embolism of the lungs. 

Results Of Embolism. — A large embolus may cause sudden 
death by occluding one of the main branches of the pulmonary 
artery, one of the coronary arteries, or a large cerebral vessel. If 
the vessel is not wholly occluded, secondary thrombosis may com- 
plete the obstruction and death may be slow. In the case of less 
important vessels merely local anemia results. This may be re- 
lieved by establishment of collateral circulation, or may cause more 
or less extensive necrosis if not relieved. The original embolus 
and the secondary thrombus may undergo softening or organization 
in the same manner as ordinary thrombi (q. v.). 

The results of occlusion of smaller vessels by emboli depend on 
the nature of the embolus. They are either purely mechanical 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 55 



when the embolus is aseptic, or septic when the embolus contains 
micro-organisms. The important mechanical result of small 
emboli is the pathologic condition called infarction. 




Fig. 4. — Anemic infarct of the 
kidney : the embolus, occluding a 
branch of the renal artery, is shown 
in the lower part of the picture 
(Perls). 



INFARCTION. 

Infarcts occur in situations in which there are small arteries 
having only capillary or at most very slight arterial anastomosis 
with neighboring arteries. Such arteries were called endarteries 
by Cohnheim. They are found especially in the kidney, spleen, 
lungs, retina, base of the brain, and 
parts of the heart. When one of 
these is occluded by an embolus in- 
farction may occur. 

Infarcts are situated in the periph- 
eral part of the organ, and are harder 
than the surrounding tissue. They 
are wedge-shaped, the base being out- 
ward toward the periphery of the 
organ. Infarcts may sometimes result 
from occlusion of a number of adjoin- 
ing arterioles or capillaries, and in this 
case are irregular in outline. There 
are two forms of infarction, the red 
or hemorrhagic, and the white or 
anemic. The former are dark red in color, and have the appear- 
ance of wedge-shaped areas of hemorrhage with coagulation. 
Anemic or white infarcts present the same general features, but 
are less elevated and are yellowish or grayish in color. They are 
frequently surrounded by a zone of congestion or hemorrhage 
(Fig. 4). 

Formation of Infarcts. — The first eifect of occlusion of an 
endartery by an embolus is stoppage of the circulation beyond the 
embolus. A wedge-shaped anemic area results. This may remain 
anemic and undergo coagulation-necrosis, with the formation of 
an anemic or ivhite infarct. In other cases, however, the vessels 
of the occluded area, after a temporary period of anemia, become 
overfilled with blood, extravasation occurs, and an hemorrhagic in- 
farct results. Various theories are offered to explain the persist- 
ence of anemia in the first case and the overfilling with blood in 
the second. In anemic infarcts the persistent anemia in some 
cases is due to thrombosis in the venules which receive the blood 
from the occluded endartery and in the anastomotic capillaries. 
At times rapid swelling of the parenchymatous cells of the organ 
compresses the capillaries and maintains the anemia. Some con- 
tend that white infarcts are frequently formed by rapid absorption 
and removal of the coloring-matter of the blood from hemorrhagic 



TEXT-BOOK OF PATHOLOGY. 



infarcts. In the latter the overfilling of the vessels results either 
from a backflow of blood from the veins (Cohnheim) or from free 
capillary-anastomosis. The latter would be especially apt to occur 
when the general or local blood-pressure was previously elevated, 
or when the lodgement of the embolus caused reflex contraction 
of the surrounding vessels, and thus overflow of blood into the 
occluded area through the capillary-anastomoses. The hyperemia 
thus produced soon leads to extravasation of blood, because the 
vessels of the occluded areas rapidly undergo degenerative changes. 
Infarcts in the lungs are nearly always hemorrhagic ; those in the 
kidneys and especially the spleen are frequently anemic. In the 
brain irregularly shaped areas of anemic necrosis (softening) are 
the usual result. 

Subsequent Changes. — In anemic; infarcts coagulation-necro- 
sis and caseation are the marked degenerative changes. The broken- 
down tissue is gradually absorbed and reactive inflammation and 
organization cause cicatrization. Not infrequently a small amount 
of calcareous matter is deposited, especially in infarcts of the lungs. 
In hemorrhagic infarcts the extravasated blood breaks up into 
pigment-matter and the tissues suffer degenerations similar to those 
seen in anemic infarcts. The final result in either case is generally 
a scar, which is pigmented in cases of hemorrhagic infarcts. More 
rarely infarcts undergo liquefaction and cyst-formation, especially 
in the brain. The infarct may become infected by micro-organisms 
after its formation and abscess may result, as in cases in which the 
embolus itself was an infectious one. 

Infectious embolism occurs in cases of purulent softening 
of thrombi, in cases of local suppuration or necrosis, in ulcerative 
endocarditis, and the like. The first effect may be the formation 
of a hemorrhagic or anemic infarct ; but the micro-organisms soon 
multiply and invade the tissues, causing suppurative or gangrenous 
processes. Metastatic abscesses are produced in this manner. 
Similar results follow when an infarct is secondarily infected. 
This is not infrequent in the lungs, where the air-passages furnish 
a ready path for the entrance of micro-organisms. 

Dust-embolism.— Small particles of coal, iron, marble, or clay entering 
the lungs in respiration may penetrate the tissues, are largely taken up by 
phagocytic cells, and for the most part are carried to the bronchial lym- 
phatic glands. If the latter are surcharged and soften, the dust-particles may 
gain access to the circulation through the efferent lymph-channels of the 
gland or by rupture of the gland into neighboring veins. More rarely dust- 
particles may enter the blood-vessels in the lungs, directly, by penetration. 
After their entrance into the blood they are deposited in the capillaries 
and substance of the liver, spleen, and bone-marrow, where they may re- 
main permanently, either free or enclosed in fixed cells, or whence they 
may be removed by wandering cells. The final discharge occurs especially 
from the lungs, the tonsils, the lymphatic structures of the intestines, and 
from the liver in the bile. 

Air-embolism.— Small quantities of air may occasion no serious dis- 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 57 



turbances; but when large quantities enter the veins the right heart is 
found full of frothy blood and the pulmonary- arterioles are occluded by 
small bubbles. Sudden death in these cases is not unusual. Some recent 
experiments in dogs seem to cast doubt on the seriousness of air-embolism, 
but the matter is not yet settled. 

Fat-embolism. — Sudden death may occur when a large number of the 
pulmonary vessels are obstructed by embolic oil-drops. When the process 
is less extensive little disturbance arises, as the oil is soon broken up into 
droplets and passes through the pulmonary capillaries, or it may be ab- 
sorbed in the lungs. 

Pulmonary infarcts maybe due to embolic occlusion of the blood-vessels, 
but also to obstruction of a bronchiole. Any kind of hemorrhagic extrava- 
sation in the lungs may assume a wedge-shape, because the area infiltrated 
is the wedge-shaped area included in the divisions of a terminal bronchiole. 
(For details, see the chapter on the Lungs.) 

Metastasis. — The process of metastasis of tumors and of infectious 
diseases is closely allied to that of ordinary embolism. Small particles of 
tumors in the one case, or of infected thrombi or tissue in the other, enter the 
blood-vessels or the lymphatic channels and are carried to neighboring or 
distant parts of the body, where they lodge in capillary-vessels. In the case 
of tumor-embolism the embolus may grow and occasion a metastatic nodule ; 
in the case of infectious processes secondary foci of the infectious disease 
result. 

THROMBOSIS. 

Thrombosis is the coagulation of blood within the blood-ves- 
sels or heart during life. At the very beginning of the process 
the formation is not a coagulum in the ordinary sense, but subse- 
quently coagulation is the essential feature. After death clots form 
within the heart and vessels, as in blood removed from the body. 

Causes. — The conditions favorable to thrombosis are alter- 
ations in the blood-current, changes in the vessel- walls, and alter- 
ations in the blood itself. For the most part two or all of these 
conditions are present in cases of thrombosis. 

Alterations in the Blood-current. — Anything which slows the 
current, such as narrowing of the blood-vessels, weakness of the 
heart, or pressure upon the vessels, favors thrombosis. Complete 
arrest of the current in a part may lead to ordinary clotting, such 
as occurs post-mortem ; but with careful precautions a vessel may 
be ligated at two points without the occurrence of clotting in the 
occluded portion — at least for a long time. Some change in the 
blood-vessel wall is generally necessary in addition. Thrombi due 
to slowing of the current are frequently seen in the heart, the ves- 
sels of the lower extremities, and in the sinuses of the brain in 
the course of exhausting fevers or other asthenic conditions. They 
are called marantic thrombi. In many of the latter micro-organ- 
isms have important etiologic relations. 

Changes in the vessel- walls play an important part. Atheroma, 
inflammatory or degenerative chancres in the vessels of areas of 
inflammation or necrosis, ligation and other traumatic injuries, and 
diseases of the endocardium are all examples of conditions leading 



58 



TEXT-BOOK OF PATHOLOGY. 



to thrombosis. In many cases of thrombosis apparently due to 
slowing of the current of blood, micro-organisms have been the 
more important factors, by causing primary infective lesions of the 
endothelium. Dilatation of the arteries (aneurysm) or veins 
(phlebectasia) or of the cavities of the heart acts largely by slow- 
ing the current of blood or by producing irregular currents. 

Alterations in the Blood. — Experimentally, thrombosis may be 
induced by injection into the circulation of extracts of the thymus 
gland, the suprarenal bodies, the testicles, and other organs. 
These extracts contain large quantities of the fibrin-ferment re- 
garded by Schmidt as an essential factor in coagulation. Patho- 
logically, it is probable that the tendency to thrombosis in typhoid 
fever, sepsis, and other diseases is due to increase of similar fibrin- 
forming factors in the blood. The name fermentation-thrombosis 
is applied in these cases. The importance of bacteria in the blood 
has been sufficiently noted above. 

According to Schmidt, coagulation is due to the reaction of fibrinogen 
(derived from the plasma) with fibrinoplastin under the influence of a fibrin- 
ferment (the two latter derived from the leukocytes). Fibrinoplastin is 
probably not essential (Hammarsten), while calcium salts are (Arthus and 
Pages). 

Pathologic Anatomy. — The appearance and construction 
of thrombi depend upon the manner of formation. 

When formed in consequence of almost complete stoppage of 
the circulation they are dark-colored, soft, red clots, similar in every 
w r ay to post-mortem coagula ; and under the microscope show fib- 
rillar fibrin enclosing mainly red corpuscles. 

Yellowish or white thrombi are formed slowly from actively 
circulating blood and are more consistent. Their composition will 
be understood from the mode of formation. In the normal circu- 
lation the red corpuscles and blood-plaques move in a column in 
the center of the stream, separated from the wall of the vessel by 
a plasmatic zone in which the leukocytes may be seen. When the 
circulation is slowed the plaques approach the vessel-wall and tend 
to adhere in small masses to any point of disease in the endothe- 
lium and also to each other. This has been termed conglutina- 
tion of the blood-plaques. Gradually the mass grows and subse- 
quently leukocytes are added. These set on foot true fibrin- 
formation or coagulation. White thrombi therefore consist of 
conglutinated plaques, leukocytes, and fibrin. They first appear as 
hyaline, viscid masses ; but subsequently become granular from 
partial disintegration. If the circulation is alternately slow and 
more rapid, distinct layers are seen in the thrombus, first dark 
colored from admixture of red corpuscles, then lighter in hue. 
Such thrombi are called stratified. If the circulation is irregular 
from dilatation of the vessels or other causes, the light and dark 
areas of the thrombus may be more irregularly disposed. 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 59 



The thrombus lirst formed is the 'primary thrombus. Subse- 
quently it extends by additions (secondary thrombus) in the direction 
of the current of blood as far as the next collateral branch of the 
vein or artery, into which the thrombus frequently extends as a 
rounded prominence. In the case of the veins a new thrombus 
may start from such projection (Fig. 5), and eventually the clot 




Fig. 5.— Thrombus in the femoral vein in a case of phlebitis (from a specimen in the 
Museum of the Philadelphia Hospital). 



may extend as far as the heart. The thrombus may be lateral — 
that is, when it lies against the vessel-wall — or obstructive, when 
the lumen is completely obliterated. In the veins small thrombi 
are frequently formed in the valvular pouches in marantic subjectSo 




Fig. 6.— Thrombosis in cardiac Fig. 7.— Branch of the brachial artery after 

chambers, showing cyst-like struct- amputation, showing vascularization of the 

ure (Orth). thrombus, Th (Weber). 

In the heart thrombi are especially common on diseased valves, in 
the auricular appendages, and in the intertrabecular spaces. They 
frequently appear as polypoid masses, and may be attached by 
slender pedicles. A curious form, called ball thrombi, is seen in 
the auricles. These are rounded clots wholly or almost wholly 
separated from the wall, and may occasion serious obstruction at 
the orifices of the heart. 

Effects. — Frequently the collateral circulation is so quickly 



60 



TEXT-BOOK OF PATHOLOGY. 



established that no untoward results are seen. When a large vein 
is obstructed venous congestion and dropsy may follow ; obstruc- 
tion of an artery causes local anemia, and subsequently, if the col- 
lateral circulation is not established, degenerations or necrosis. 
Thrombotic obstruction of small arteries may cause hemorrhagic 
infarction. Embolism and general pyemia result from softening 
of the thrombus. 

Subsequent Changes. — After their formation all thrombi 
contract. In this way the red forms may become light colored by 
extrusion of the red corpuscles. In small vessels red thrombi often 
become light colored by removal of hemoglobin and a species of 
hyalin-transformation. These may have the appearances of white 
thrombi and are only distinguished by careful examination. 

After the thrombus has contracted it may undergo various 
degenerative changes. Frequently the white corpuscles, plaques, 
and fibrin are broken down into an emulsion by liquefaction- 
necrosis and fatty degeneration, and the red corpuscles converted 
into granular pigmented masses. These softened portions are 
swept into the circulation and occasion embolism. Frequently 
this form of simple softening occurs in the center of large thrombi 
and gives rise to cyst-like formations (Fig. 6). 

A more serious form of softening occurs when the thrombus is 
infected by micro-organisms. In this case true purulent softening 
takes place, and the wall of the blood-vessel shares largely in 
the suppurative processes. This form occurs especially in the 
thrombi blocking blood-vessels of suppurating or necrotic tissues. 
General pyemia and infectious embolism result. 















■ 






Ipll 













Fig. 8.— Canalization of a thrombus (Karg and Schmorl). 



A more favorable termination of a thrombus is calcification. 
This is most frequent in the clots in dilated veins, the calcareous 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 61 



thrombi being known as phleboliths. Arterioliths and cardioliths 
are rarely met with. 

Organization of the thrombus may result from the irritation 
it occasions. New blood-vessels and proliferating connective-tis- 
sue cells spring from the vasa vasorum and lining membrane of 
the blood-vessel as well as from endothelial cells covering the throm- 
bus, and penetrate the thrombus (Fig. 7). From these organi- 
zation proceeds as elsewhere, and as it advances the thrombus 
itself is absorbed. Finally, the clot is fully replaced by connec- 
tive tissue enclosing a small amount of blood-pigment or calcined 
remains of the thrombus. The blood-vessel may be converted into 
a solid fibrous cord, or may be distorted and narrowed by bands of 
connective tissue in the interior. Sometimes after partial vascu- 
larization of a thrombus small vessels running parallel with the 
lumen of the obstructed vessel become dilated and thus partly re- 
establish the channel. This is termed canalization of the throm- 
bus (Fig. 8). In other cases canalization may begin as a process 
of simple softening. 

EDEMA. 

Definition. — The term edema is applied to a condition in 
which the liquid within the tissues is increased in quantity. 

Etiology. — It is primarily necessary to understand the methods 
by which the liquids normally present in the tissues escape from 
the blood-vessels, their original source. 
» 

Several processes are concerned in this escape of fluid. In the first 
place, the pressure of the blood serves to cause a certain amount of direct 
filtration, just as liquid enclosed in tubes of permeable animal-membrane 
escapes when the pressure outside is less than within. In this process of 
direct filtration the state of the tissues themselves plays a part. If the 
normal elasticity of the tissues and degree of pressure of the liquid in the 
interstitial spaces are lowered, liquid escapes through the capillary-walls 
to equalize the pressure. A second process at work is that known as 
diffusion or osmosis. In this there is an exchange between the blood and 
the tissue-liquids, certain substances being taken into the blood in ex- 
change for water and other constituents of the blood-plasma. The liquid 
thus discharged from the blood-vessels enters into the metabolic activity 
of the tissues to a greater or less degree, is somewhat altered in character, 
and the surplus is carried off in the lymphatic capillaries as lymph. Cer- 
tain physiologists (Heidenhain et al.) believe that there is a farther and 
very important factor of a vital sort. This is described as an active secre- 
tory function of the endothelial cells of the capillaries and lymphatic 
spaces ; so that, according to this view, lymph-formation is in a measure 
at least a direct secretion. This view, though not generally accepted, is sup- 
ported by many facts. 

Briefly, then, lymph-formation may be described as the escape of water 
and other substances through a more or less permeable membrane, the 
capillary- walls, in consequence of direct filtration, osmosis, and probably 
secretion. The quantity present in the tissues depends upon the quantity 
escaping from the blood-vessels and the amount carried away by the 
lymphatic circulation. 



62 



TEXT-BOOK OF PATHOLOGY. 



The causes of increased accumulation of liquid in the tissues 
may then be readily determined. Among these are (a) increase 
of blood-pressure, or (6) decrease of tissue-elasticity and pressure ; 
(c) alterations of the blood rendering it more diffusible, or (d) of 
the liquids in the tissues increasing the osmotic power of these ; 
(e) increased permeability of the walls of the blood-vessels; (/) 
obstruction to the flow in the lymphatic vessels. These causes 
will be considered separately with reference to certain well-known 
clinical types of edema. 

(a) Increased blood-pressure always occasions increased escape 
of liquid from the vessels (transudation) and thus increased forma- 
tion of lymph. In active hyperemia with excess of pressure the 
amount of liquid rarely becomes so great that the lymphatic ves- 
sels cannot carry it off, and edema does not therefore occur. In 
passive congestions, however, as in heart-disease, pressure upon 
veins, etc., the escape of liquid becomes more rapid and copious, 
and the lymphatic circulation is insufficient. Edema or dropsy 
results. In this process of direct filtration the transudate consists 
mainly of the water and saline constituents of the plasma and to a 
relatively small degree of the albuminous constituents. 

(6) Decreased tissue-elasticity and pressure is rarely a factor of 
prime importance, though it may be a contributing cause in many 
cases. In one class of cases termed oedema ex vacuo it is the 
principal cause. In these cases liquid escapes from the blood- 
vessels to fill a space left vacant by disease or atrophy of tissue- 
elements. This is frequently seen in the subarachnoid spaces of 
the brain and in other parts of the central nervous system. 

(c) Alterations of the blood, though theoretically very impor- 
tant as direct causes, probably act indirectly. It has been found 
by experiment that artificial hydremia, even though combined 
with considerable increase of the bulk of blood, does not cause 
edema unless by some means the walls of the blood-vessels have 
been injured. It is probable, therefore, that the edema of anemic 
and marantic persons is similarly due to increased permeability of 
the vessels. This in itself might occasion edema, though the 
degree is probably greater as a consequence of the anemic state of 
the blood. The vascular disease itself is probably in some way 
(perhaps by the action of circulating toxic substances) brought 
about by the condition of the blood. 

(d) Alterations of the liquids of the tissues may, conceivably, 
occasion increased diffusion of liquid, but practically little is 
known of the operation of this element. There are, however, 
certain cases in which disturbed metabolic activity of the tissues 
seems to alter the tissue liquids in such manner as to favor the 
development of dropsy. 

(e) Increased permeability of the capillary -walls is of great 
importance and probably plays a part in every case of edema. Ex- 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 63 



perimentally it is easy to prove that this factor alone may cause 
pathologic transudation. Applications of heat to a part or the 
introduction of poisons capable of causing disease of the walls of 
the blood-vessels may thus occasion edema. Clinically this factor 
is of importance in the edema of Bright's disease. Formerly the 
dropsies of renal disease were attributed to hydremia, but the 
experiments cited above show this factor to be insufficient.- On 
the other hand, changes of the vascular system are known to occur 
in Bright's disease, and particularly in cases usually attended with 
marked edema (glomerulonephritis). Changes in the blood may, 
of course, contribute, as may also stasis due to cardiac weak- 
ness. 

Disease of the capillary-walls is also an important cause of 
edema in and about areas of inflammation (inflammatory edema). 
In these cases the toxic causes and products of inflammation doubt- 
less attack the walls of the vessels and render them more porous. 
Such edema may occur only in the vicinity of an inflamed area, or 
may be widespread. Thus in some cases edema of the lungs and 
other internal organs may be occasioned by bacterial toxins derived 
from a distant focus of infection. 

Cases of hereditary edema have been described. These may 
owe their origin to a congenital excess of vascular permeability. 

Finally, there are cases of edema in which the nervous system 
seems to exercise an influence. Among these are the dropsies 
attending cases of neuritis, neuralgia, or organic diseases of the 
cord. li\ these instances changes in the blood-vessels and per- 
haps in the tissue-elasticity may be important causes. An inter- 
esting form of this sort is that known as angioneurotic edema, in 
which local edema of various forms (often as giant-urticaria) makes 
its appearance under the influence of nervous irritations. 

(/) Obstruction of the lymphatic circulation does not ordinarily 
occasion edema, because the collateral circulation is sufficient to 
carry away the lymph. When, however, a larger trunk, especially 
the thoracic duct, or numerous smaller lymphatics are obstructed 
edema may result. This is observed in the chylous ascites due to 
obstructions of the thoracic duct and in the edema of elephan- 
tiasis. 

Pathologic Anatomy. — Edema may take various forms 
according to its situation. In some cases it is localized, affecting 
a limited part of the body, as a single organ or member. In other 
cases it is widespread in the subcutaneous tissues and skin, when 
the term anasarca is applied. It may occur in the serous cavities 
in the form of serous transudates (hydrothorax, ascites, hydro- 
pericardium, etc.). 

The liquid itself varies in character according to the cause. In 
the pure transudates due to increased filtration the liquid is watery, 
low in specific gravitv (below 1016), and comparatively poor in 



64 



TEXT-BOOK OF PATHOLOGY. 



blood-corpuscles and albuminous constituents. In cases in which 
disease of the vessel-walls has played a large part in the causation, 
especially in the inflammatory edemas, the liquid is more dense 
and contains more corpuscles and albuminous bodies. 

The transudate first occupies the lymph-spaces or interstices of 
the tissues, causing a more or less uniform swelling and bogginess. 
The tissue pits on pressure, and on section more or less abundant 
liquid exudes. The solid organs (kidneys, liver) are lighter in 
color, less dense, and more moist on section than normal ; but the 
appearances of edema are here less characteristic than in the sub- 
cutaneous or submucous tissues, or in the softer organs like the 
lungs and brain. 

Microscopically the tissue-elements are seen to be pushed apart 
by the transudate, and in some cases the cells themselves may be 
diseased (see Dropsical Infiltration). 

Results of Edema. — The function of edematous parts is 
necessarily impaired. Sometimes serious consequences ensue, as 
in the case of edema of the epiglottis, the lungs, or the brain. 
Secondary changes may occur in parts the seat of continued edema. 
Among these are various degenerations of the cells and a productive 
change in the connective tissues. The latter is well illustrated in 
the sclerotic change in the subcutaneous tissues of long-standing 
dropsy, elephantiasis, etc. 



CHAPTER IV. 

RETROGRESSIVE PROCESSES. 
ATROPHY. 

Definition. — Atrophy is a condition in which a tissue or organ 
undergoes a more or less uniform diminution, without definite 
disease of its constituent parts. It is extremely difficult to draw 
a sharp line between atrophy and degeneration. Frequently one 
of these conditions merges in the other. 

Hypoplasia. — This term is applied to a condition in which certain 
organs or tissues fail of their normal development. Thus the heart and 
blood-vessels and the internal genitalia have been found incompletely 
developed in some cases of chlorosis ; and similar conditions have been 
found in other diseases or apart from manifest disease. It is difficult to 
determine in some cases whether the lack of development is purely the 
result of deficiency in the developmental processes or the result of congeni- 
tal disease. Thus in the state called infantilism, in which the body as a 
whole remains undeveloped, there is doubtless a relationship with cretinism, 



DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 65 



and primary disordered action or deficiency of the thyroid gland is the 
underlying cause. Occasionally an organ or part of the body is entirely 
wanting. To this condition the name aplasia is given. 

Btiology. — The causes of atrophy may be varied. It occurs 
as a result of want of functional demand, as in the atrophies 
affecting palsied limbs ; and sometimes as a result of disturbances 
of the trophic nervous system, as in diseases of the anterior horns 
of the spinal gray matter. In the latter instances lack of -use is a 
contributing cause. In the involution processes of old age there 
is more or less general atrophy, which might be designated as 
physiologic. Similar normal or physiologic atrophy occurs in 
certain organs before the general manifestations of old age. Thus 
the atrophy of the thymus-gland in early childhood and of the 
genital organs at the menopause are instances of cessation of func- 
tion, and consequent or concomitant atrophy of physiologic char- 
acter. Atrophy may be more definitely pathologic, and the 
result of distinct causes, such as want of local or general nourish- 
ment by occlusion of the vessels, pressure, etc. In these cases the 
process may be purely atrophic, or there may be distinct degenera- 
tive disease of the cells with diminution of bulk. 

Pathologic Anatomy. — Atrophy may be simple or numerical. 
In the former kind, to which the term true atrophy might also be 
applied, the individual cells decrease in size without manifest dis- 
ease ; in the latter the cells are reduced in number, and are usually 
first altered by some form of degenerative disease, so that the proc- 
ess is not, strictly speaking, true atrophy. T< , - ..^ r _ 
The parenchyma of organs suffers first and \ : . 1 

most characteristically, the connective tissues | \ ' \ § |H 
remaining unaffected or even undergoing hy- ' i % 

perplasia. In true atrophy the cells may ; f j. 

present no definite alteration, excepting per- J ' % -v 
haps slightly increased pigmentation. This i ! •/ 
is sometimes due to the fact that the normal / ... | , i 
pigment of the cell does not suffer reduction i 
as do the other constituents of the cell, but :p j r '" " J 1 ^' 

in other cases there is actual deposition of FlG - t 9 ^he2n n m a us?re by °* 
pigment (hematogenous). Cases of the latter 

kind are designated as brown atrophy (Fig. 9). This is seen most 
strikingly in the heart-muscle in advanced old age or in persons 
dead of some chronic cachectic disease. In some of the conditions 
generally described as atrophy the cells show degenerations of 
various forms, such as cloudy swelling, coagulation-necrosis, fatty 
degeneration with vacuolization, and other gross alterations of 
structure. 

Secondary degenerative changes may occur in the connective 
tissues after the parenchyma-cells have become atrophic. Thus, 
after the physiologic atrophy of the thymus-gland has occurred 

5 



66 



TEXT-BOOK OF PATHOLOGY. 



the connective tissues of the gland and of the surrounding parts 
become converted into fatty tissue. In other cases myxomatous 
change may be observed. 

Organs which have undergone atrophy are often quite irregular 
on the surface from unequal involvement of the different con- 
stituents. The consistency may be little changed or may be 
greatly reduced, particularly when some form of cellular degenera- 
tion is present. On the other hand, the organ may be hard and 
tough from secondary hyperplasia of the connective tissue. The 
capsule is generally wrinkled from the shrinkage of its contents, 
and secondary thickening is not unusual, especially in the heart 
and spleen. The color of the organ, like that of the individual 
cells, often becomes darker than normal and may be decidedly 
changed in brown atrophy. 

In cases of pressure-atrophy various distortions of the affected 
organ may be observed. These are particularly marked in the 
livers of women who have laced excessively. The right lobe of 
the organ often presents a deep groove or furrow corresponding 
with the lower border of the ribs, and each of the ribs with which 
the organ comes in contact may cause a depression. 

Pathologic Physiology. — The function of an atrophic 
organ is necessarily impaired. In the atrophies of old age this 
may be of little consequence, as the functional demand grows less 
and less. In premature atrophies general as well as local disturb- 
ances may occur. These disturbances vary with the varying 
functions of the organs, and will be separately discussed. 

THE DEGENERATIONS. 

The general term degeneration is applied to. changes in the 
tissues by which their integrity is altered in the direction of 
lowered vitality. There may be a conversion of the protoplasm 
of the cell into substances abnormal to it either in kind or quantity. 
This is termed degeneration in a narrower sense. In a second 
class there are deposited in the cell, from the blood or other fluids 
of the body, substances abnormal to the cell in kind or quantity. 
The name infiltration is applied to these processes. In individual 
cases it is often difficult to distinguish between the two varieties. 

CLOUDY SWELLING. 

Definition. — Cloudy swelling, also termed albuminous infil- 
tration and parenchymatous degeneration, may be defined as an 
edema of the cellular protoplasm, with alterations in the proto- 
plasmic proteid and the production of opacity. 

Etiology. — Cloudy swelling is an almost universal accom- 
paniment of inflammations. Circulatory disturbances (anemia) 



RETROGRESSIVE PROCESSES. 



67 



were formerly supposed to be important, but are now considered 
to be of little significance. Fever per se can produce cloudy swell- 
ing, probably not so much the result of the simple degree of heat 
as of metabolic disturbances induced thereby. The niost frequent 
cause of cloudy swelling is intoxication, either by bacterial toxins, 
as in the various infectious conditions, or by innumerable organic 
and inorganic substances. Cloudy swelling is also caused by nu- 
tritional disturbances ; starvation of an organ will produce it as the 
first stage of atrophy ; and, on the contrary, the cells may in other 
cases be so overloaded with nutritional substances as to become 
temporarily transformed into this condition, as in the glandular epi- 
thelium of the liver during active digestion. It is further known 
that excessive cellular activity may result in a cloudiness of the 
protoplasm, as in the kidney and in glands excited by nervous 
stimulation. These latter processes should be viewed as normal 
phenomena, analogous to the physiologic fatty degenerations. 



% A 



* *t * 



Fig. 10.— Cloudy swelling and necrosis of the epithelial cells of the renal tubules, due to 
sublimate-poisoning (Karg and Schmorl). 



Pathologic Anatomy. — The swollen cells present a fine 
opacity which under high powers is seen to be due to the presence 
of diffused refractile granules (Fig. 10). The normal protoplasmic 
granulations have disappeared ; in muscle-fibers the striations are ob- 
scured or obliterated. Vacuolation may be seen in the late stages. 
The cell-wall becomes indistinct, so that the cells appear to have 
coalesced. The nuclei may be little altered. Generally the 
chromatin becomes diffusely stained ; it may elect the acid-stains 
or may refuse all staining. Marked nuclear degenerations are 
not seen in simple cloudy swelling, or at least very rarely. In 
late stages the entire cell may lose its normal reactions to stain- 



68 



TEXT-BOOK OF PATHOLOGY. 



ing-reagents. The distinctive granules are not soluble in alcohol 
or ether, but are dissolved by acetic acid and alkalies. 

The large glandular organs, the liver and kidneys, illustrate 
the condition exquisitely. The entire organ is symmetrically 
swollen ; the general consistency perhaps a little decreased. On 
section the surface may be found a little moist and the paren- 
chyma protrudes. The color is an opaque pallor, suggesting the 
appearance of boiled flesh. 

Seats. — The glandular epithelia (liver and kidney) and the 
muscle-fibers are the striking seats of this degeneration. 

Pathologic Physiology. — The opacity seems to be due to 
a coagulation or precipitation of a part or all of the protoplasmic 
proteid. Some systematic writers have attempted to divide it into 
two groups : albuminous infiltration, in which the material has 
been deposited in the cell and then been precipitated ; and albu- 
minous degeneration, in which the inherent cellular proteid has 
been precipitated. It is doubtful whether this division is justified. 
The chemic relations are entirely obscure. It is as yet incompre- 
hensible how bacterial toxins, themselves apparently proteids, can 
precipitate other and higher proteids. In the case of inorganic 
poisoning (metallic salts, acids) the process is more readily under- 
stood. The swelling is probably a simple edema, due, it may be 
inferred, to disturbed osmotic relations. 

The function of organs is more or less profoundly disturbed by 
this form of degeneration. Complete recovery is easy and fre- 
quent. If, however, the causes persist, the cells pass into other 
degenerations, usually fatty metamorphosis. 

FATTY INFILTRATION. 

Definition. — Fatty infiltration is the deposition of fats derived 
from the circulation in cells and tissues which normally contain 
none, or the deposition of an excess of fats in cells and tissues 
which normally contain such. 

Etiology. — Fatty infiltration may be physiologic or patho- 
logic in its origin. In conditions of general obesity the regular 
consumption of excessive quantities of nourishment may lead 
to the most marked degrees of fatty infiltration.; an inherited 
predisposition and lack of exercise acting as contributing causes. 
In rare instances it seems possible that with the normal physio- 
logic diet persons of exceptional digestive power and living 
under conditions which restrict combustion may become affected 
with pathologic fatty infiltration. The condition may occur 
during pregnancy, and is frequent at the menopause. In a 
large class of cases an abnormal diet, or the presence in the 
diet of substances which tend to the formation of fats, such as 
alcohol, are responsible for the condition. It is doubtful whether 



RETROGRESSIVE PROCESSES. 



69 



poisons produce general fatty infiltration ; they frequently, how- 
ever, indirectly produce local or visceral infiltrations. In cachexias 
certain organs may become loaded with fats, as is sometimes seen 
in the liver in phthisis. In carcinoma the cells of the neoplasm 
may become infiltrated with fats. In organic diseases of the ner- 
vous system accompanied by extensive disintegration of myelin, in 
bone-diseases, and even following fractures of or operations on 
bones, the liberated fats are taken up by the circulation and 




deposited in susceptible localities. There is a rare form probably 
entirely of senile origin, and also a type which appears at puberty. 
Of general diseases that may cause general fatty infiltration, chlo- 
rosis and diabetes may be mentioned. Fats may be deposited 
locally as substitution-tissue, as in the capsule about sclerosed 
kidneys, in the place of atrophied muscular fibers, in the bones, 
and about areas of local disease. The protective areas of fibrous 
tissue which wall off pathologic processes of various kinds may 
become extensively infiltrated. 

Pathologic Anatomy. — Normal tissue plus fat describes 
the appearances. The fat may be diffuse, in localized areas, or in 
streaks along the planes of fibrous tissue. The appearances natu- 
rally vary with the tissue affected. The connective tissue rather 
than the parenchyma usually displays the disease. Microscopically 
the fat-drops are seen within and without the cells. Without the 
cells they are most prominent along the fibrous strands, under the 
endothelial membranes, about the lymph-channels, between the 
muscular fibrillaB, and to a marked extent just beneath the true 
skin, and indeed about all fasciae. In the kidney the collections 
are between the tubules ; in the liver, in the fibrous trabecule, 
but especially in the hepatic cells ; in the heart, underneath the 



70 



TEXT-BOOK OF PATHOLOGY. 



serosa and between the bandies of fibers. Within the cells, and 
this is most marked in glandular epithelial cells, the fat is seen 
as distinct drops within the cell-wall. The fat-drops are always 
of considerable size, and soon run together, forming one drop, 
which pushes the protoplasm and nucleus against the cell-wall. 
The nuclei are usually normally distinct and stain well ; the 
cell-protoplasm is clear and presents its normal granules ; the cell- 
wall is intact, though often bulging to accommodate the excess of 
contents. In rare, prolonged, and extreme instances the bulk of 
the fat may be such as to interfere with the functions and nutrition 
of the cells, whose nuclei and protoplasm will then show patho- 
logic alterations. Crystalline formations, as of margarin and 
cholesterin, and tiny balls of lecithin may be present, but are 
more often seen in fatty degenerations. The fat may be stained 
with osmic acid or sudan III. 

Seats. — The favorite seats of fatty infiltration are the subcu- 
taneous and subserous tissues, the mesenteries and omentum, 
along the fasciae, between the muscles, about the kidneys, and in 
the liver and heart. The lungs and central nervous organs are 
rarely and only slightly affected. 

Pathologic Physiology. — I have attempted to define this 
condition rigidly as an infiltration of fat into cells or tissues, dis- 
tinct from formation of fat in them. Confessedly in individual 
cases the separation may be impossible ; all doubtful cases are 
probably degenerative. Infiltration arises whenever there is an 
abnormal quantity of fat in the circulation ; the causes of this 
were pointed out in the etiology. Infiltration into imperfect or 
diseased cells may, however, occur with only normal quantities of 
circulating fats ; this is probably the explanation of many of the 
local varieties. All cells and tissues are not of the same degree 
of susceptibility ; when, therefore, isolated areas occur in unusual 
localities a pre-existing disease should be suspected. The mech- 
anism of deposition is not well understood ; it is perhaps effected 
by circulating cellular carriers. 

Unless very extreme, fatty infiltration does not seriously em- 
barrass the functions nor threaten the existence of tissues, and 
complete recovery and restitution are the rule. It may, however, 
lead to secondary degenerations, which, particularly in the heart, 
may be of serious consequence to the organ. 

FATTY DEGENERATION. 

Definition. — This is defined as a metamorphosis, the conver- 
sion of the cellular protoplasm into fat. The classic physiologic 
illustration is the fat-production in the secretion of milk. The 
nature of this process has not, however, been certainly determined. 
The majority of secreting cells neither die nor show pathologic 



RETROGRESSIVE PROCESSES. 



71 



alterations ; while in the case of such as are cast off, as colostrum- 
cells, it has not been shown that their fat was not an infiltration. 

Etiology. — Fatty degenerations frequently follow upon cloudy 
swelling, and the causes detailed for the one apply also to the other. 
Of all agents, poisons are the most important. These may be me- 
tallic, as mercury, arsenic, lead, phosphorus — indeed most of the 
metals. Compounds which directly bind the hemoglobin or reduce 
it, or break up the red corpuscles, likewise produce it. Such are 
carbonic oxid, chlorates, pyrogallic acid, some coal-tar compounds, 
etc. Certain poisons, like chloroform, ether, iodoform, and the 
acids, seem to act directly on the cell-nutrition. In the case of 
most of these substances it seems to have been shown in more or 
less accurate chemical studies that the poison acts by disturbance 
of the gaseous cellular metabolism. The toxins of bacteria are 
causes of importance, but their mode of action is not clear, and the 
analogy with the metallic poisons which naturally suggests itself 
has not been made out. In all anemias and cachexias fatty de- 
generation is common ; it is rare in uncomplicated chlorosis. The 
degeneration in these pases was formerly regarded as due to sub- 
oxidation. Since, however, it has. been shown that no sulfoxida- 
tion occurs in such chronic anemias, the degeneration may best be 
classed as toxic. It seems possible, however, that extreme hemor- 
rhage can produce fatty degeneration by suboxidation. Metab- 
olic diseases can also produce it, as is sometimes seen in diabetes. 
Fever can produce it, but the temperature must be high and 
prolonged. 

Local fatty degenerations may be caused by local disturbances 
in nutrition, if not too sudden. This is seen in cases of con- 
gestion, thrombosis, embolism, atheroma, in tumors, and in tuber- 
cular and syphilitic deposits. The fatty changes of senility are 
probably of like origin. In the involution of tissues, as in the 
thymus, corpus luteum, uterus, etc., fatty degenerations are com- 
mon. Trophic disturbances produce the degeneration, as is seen 
in the voluntary muscles. In many pathologic processes, as in 
caseation, liquefaction-necrosis, and the resolution of pneumonia, 
this metamorphosis plays an important role. In rare instances, as 
mentioned, fatty infiltration may pass into fatty degeneration. 
The transformation en masse of tissue into fat, as in fat-necrosis, 
should not be termed fatty degeneration. 

Pathologic Anatomy. — Organs the subject of marked fatty 
degeneration are often somewhat increased in size : to this, how- 
ever, there are many exceptions ; a notable one is acute yellow 
atrophy of the liver. The consistency is usually lessened, though 
associated fibrosis may render the affected part abnormally dense. 
The specific gravity of* the tissue is notably reduced. In the ner- 
vous system and in caseation and allied conditions liquefaction 
may occur. The color in typical instances is a pale yellow ; the 



72 



TEXT-BOOK OF PATHOLOGY. 



existence and degree of congestion, pigmentation, or jaundice, will 
obviously alter the color. The areas of degeneration may be uni- 
form or isolated. In the heart and liver particularly streaks or 
irregular areas may produce a mottled appearance. On section 
free fat may drip from the knife and cut surface ; in other cases 




no fat-droplets can be seen macroscopically. In rare instances 
fat-crystals may be visible to the naked eye. 

Microscopic Appearances. — The parenchyma-cells are first and 
most extensively affected, though the connective tissue may be- 
come involved. The cells are usually somewhat enlarged. The 
natural granules of the protoplasm disappear, and 
| * in their stead are fine dark granules, which usually 

?J* stain black with osmic acid (Figs. 12, 13), and 
which are dissolved by alcohol, ether, etc., but 
not by acetic acid. A peculiar reaction of the 
-. ,< • granules is their staining with fuchsin (fuch- 
sinophile granules). Usually the granules are 
very fine and only slightly refractile ; they may, 
however, be large, and considerable droplets may 
^ appear or the entire cell become one large fat- 

drop, as in fatty infiltration. The nuclei in many 
cases of moderate degree show no changes ; later 
in the process, however, the chromatin becomes 
diffused and refuses to stain and the nucleus may entirely disap- 
pear. Large hyalin balls may form inside the cells ; these stain 
with acid-stains. The cell-membrane sooner or later breaks down, 



Fig. 13.— Fatty de- 
generation of the 
heart-muscle. 



RETROGRESSIVE PROCESSES. 



73 



and the fatty contents and detritus fill the space. Cholesterin, 
lecithin, and fatty crystalline formations are often seen. 

Seats. — Fatty degeneration occurs in nearly all tissues. The 
epithelial structures, especially the liver and kidneys, the heart- 
muscle, and the central nervous organs are the tissues most fre- 
quently affected. As before stated, interstitial as well as paren- 
chymatous tissues may be involved. The cellular constituents of 
exudates and transudates are also liable to the change, and the 
liquid may thus present the appearance of an emulsion. 

Pathologic Physiology. — The manner of occurrence of 
fatty metamorphosis is as yet entirely obscure. If it were proved 
that fats can be formed out of proteids, this fact would warrant 
the simple explanation that in fatty degeneration the protoplasmic 
proteid is directly converted into fat. Certain evidence of this has, 
however, never been presented, and our reactions for fat are too un- 
reliable to warrant deductions from simple microscopic studies. It 
has become apparent that the old and still largely accepted phys- 
iologic theory has never been demonstrated, even though it be 
true. No one has as yet produced fat in an animal fed on proteids 
entirely freed from fats and carbohydrates, and in the experi- 
ments with meats which contain both it has not been shown that 
any carbon-retention was unaccompanied by nitrogen-retention 
and that the carbon was retained in the form of fats or glycogen. 
It is, of course, quite possible that the proteids may be directly 
converted into fat, and in recent experiments upon starving frogs 
poisoned with phosphorus this was apparently demonstrated ; but 
even in these experiments it is likely that the glycogen of the 
liver was the source of the fat produced. 

Unlike fatty infiltration', fatty degeneration tends to cell-death, 
as must in the nature of things be obvious, for it is an expression 
of cell-disease. Mild grades with the preservation of the nuclei 
undoubtedly admit of recovery ; severe grades go on to total 
necrobiosis. The function of the cells is, of course, disturbed. 
This may be in the direction of simple reduction of function, or it 
may cause distinctly abnormal activity with pathologic metabolic 
products. 

THE ALBUMINOID DEGENERATIONS. 

The amyloid, hyaline, mucoid, and colloid degenerations rep- 
resent proteid metamorphoses which are closely related. In 
typical instances they can be quite clearly differentiated from each 
other, and for the sake of clearness and convenience they will be 
separately described. It must be understood, however, that the 
products are closely related substances whose chemical character- 
istics and relations are not clear, and which cannot in many cases 
be distinguished. 



74 



TEXT-BOOK OF PATHOLOGY. 



AMYLOID DEGENERATION. 

Definition. — This consists in the appearance in tissues of 
amyloid material ; whether formed in loco or deposited is not quite 
clear. Amyloid seems to be a combination of chondratin-sulphuric 
acid with a proteid. 

Etiology. — The common conditions under which amyloid 
degeneration arises are suppuration and ulceration. In tubercu- 
losis, especially of the lungs and skeleton, and particularly in cases 
of mixed infection, and in syphilitic ulceration are found the con- 
ditions most favorable to its production. It occurs, however, in 




Fig. 14.— Amyloid degeneration of the kidnev, showing amyloid substance in the walls 
of the blood-vessels of the glomerulus at b, and hyaline tube-casts in the renal tubules 
at g (Ziegler). 

ulcerations of various sorts, in cutaneous ulcerations, in gastro- 
enteritis, in connection with neoplasmic necrosis, in actinomycosis. 
Earely it occurs under conditions of cachexia Avithout suppuration, 
as in cancer, malaria, leukemia. In a few instances it occurs 
Avithout any apparent cause. 

Local amyloid formations are probably in no wise connected 
with the general condition and undoubtedly are often entirely 
physiologic. 

Pathologic Anatomy. — In marked instances the organs are 
enlarged, and their specific gravity increased. On section the 
tissue is firm ; the cut surface is smooth and neither contracts nor 



RETRO GRESSI VE PR CESSES. 



75 



extrudes. The consistency varies with the coexistence and degree 
of fibrosis, fatty degeneration, etc. Amyloid substance is more 
inelastic than any other degenerative material. The color of the 
organ is usually pale, but may obviously be altered by congestion, 
pigmentation, or fatty degeneration. The amyloid substance itself 
has a glistening, waxy, translucent appearance which is almost 
pathognomonic. This waxy appearance is not always uniform. 
Mild or even moderate degeneration may not present macroscopic 
appearances ; in fact, apparently quite normal tissues may be 
highly amyloid microscopically. The special appearances in 
various organs will be described in the appropriate chapters. 

Microscopic Appearances. — The favorite seats are the intima and 
media of the blood-vessels, the adventitia being rarely affected, the 
endothelium apparently never. The fixed connective tissues of the 
organs are the parts affected, the wandering cells and leukocytes 
being rarely involved. Muscle-cells are undoubtedly susceptible; 
but recent studies seem to show that glandular and lining epithe- 
lium is never involved. Such cells may, and often do, show fatty 
or other degenerations or necrosis, but the presence of amyloid 
substance within their protoplasm has not been shown. The sub- 
stance appears as irregular clumps or streaks in the interstitial 
tissues, often compressing the cells and blood-vessels. It presents 
a glistening homogeneous appearance. The cells usually present 
evidences of atrophy and other degenerations. In the renal glome- 
ruli and in the Malpighian corpuscles of the spleen the appear- 
ances are perhaps most distinctive. Without staining amyloid 
degeneration cannot akways be distinguished from other degenera- 
tions ; indeed, not always with staining reactions. The substance 
is highly resistant to bacterial decomposition and to digestion. 

Reactions (see also below). — The gentian-violet reaction seems 
to be the most invariable. In sections of tissue fixed for micro- 
scopic study gentian-violet colors the normal tissues blue ; the 
amyloid substance is a light pink or red. Iodin-green gives a 
similar red reaction. A mahogany-red reaction with Lugol's 
solution of iodin is quite constant, but fails in the isolated amy- 
loid bodies. It is easily obtained in fresh specimens. The red 
color is changed to a blue by treating with sulphuric acid or 
chlorid of zinc. 

Seats. — In the order of frequency amyloid degeneration affects 
the kidney, liver, and spleen, then the larger blood-vessels, the 
intestinal mucosa, the lymph-glands, the skeleton, the adrenal 
bodies, and the heart. It rarely affects the pulmonary mucosa, the 
bladder and genitalia, the thyroid body, the voluntary muscles, 
and, apart from the local amyloid bodies, the nervous system or 
the integument. 

Local Amyloid Formations. — These occur in the nervous system, 
especially in advanced years and in scleroses, grouped about the 



76 



TEXT-BOOK OF PATHOLOGY. 



blood-vessels, most marked in the posterior cord and in the brain ; 
in the prostate gland ; about inflammatory areas ; in infarcts ; in 
granulomata, especially syphilis ; and in neoplasms. They present 
themselves as small round bodies which usually have a concentric 
arrangement resembling starch-granules. They do not usually 
present the typical amyloid reactions ; often they react more like 
hyaline substance, and indeed the blood-vessels in their situation 
seem especially affected with hyaline change. The special appear- 
ances and reactions of the amyloid bodies of the nervous system 
will be described in connection with neuropathology. 

Pathologic Physiology. — As stated, amyloid substance 
seems to be a combination of chondratin-sulphuric acid with a 
proteid. It is composed of hydrogen, nitrogen, carbon, and sul- 
phur, and is insoluble in weak alkalies. Chondratinic acid is 
normally present in bones, cartilages, and elastic tissue. It seems 
to have been shown that an amyloid-like substance exists in the 
elastic coat of the blood-vessels — perhaps a different combination 
of chondratinic acid. Our present knowledge suggests that amy- 
loid substance is not entirely abnormal, but rather an abnormal 
combination of normal substances. It seems to result from pro- 
teid alterations in connection with the pathologic processes already 
detailed. That bacterial influences are not necessary is suggested, 
though not proved, by the fact that amyloid change has been pro- 
duced by long-continued aseptic suppuration induced by turpentine 
injections. 

Amyloid substance cannot be removed, but does not of itself 
compromise life. It may become transformed into typical hyaline 
substance. Amyloid degeneration interferes with functional activ- 
ity by pressure upon the parenchyma and by vascular disturb- 
ances. By its situation in the blood-vessels it may occasion 
thrombosis. 



HYALINE DEGENERATION. 

Definition. — This is a retrogressive process consisting in the 
appearance of a homogeneous proteid substance of obscure nature. 
It is closely allied to amyloid, mucoid, and colloid degeneration, 
and can certainly pass into each of them. The hyaline change of 
epithelium of older authors is now by general consent classed as 
a mucoid transformation. 

Btiology. — Hyaline degeneration occurs under the following 
pathologic circumstances : in the muscles during infections and 
septic processes and following traumatism ; in intoxications, as by 
lead ; in interstitial hemorrhages and hematoma ; in struma ; in 
cicatrices ; in the blood-vessels in old age, arteriosclerosis, or aneu- 
rysm ; in all forms of arteritis, especially of the nervous system ; 
in the endocardium and cardiac valves in all diseases affecting 



RETROGRESSIVE PROCESSES. 



77 



them ; in the granulomata ; in neoplasms, especially cylindromata 
and keloids ; in the lungs in pneumonia ; in the kidneys in nephri- 
tis ; and in all conditions of coagulation-necrosis and fibrinous 
exudation, for in these processes hyaline degeneration, seems to be 
a factor. 

Pathologic Anatomy. — Hyaline change is not usually mas- 
sive enough to be macroscopically appreciable. When so, the organ 
or tissue is enlarged, dense, and presents a pale, homogeneous, 
opaque appearance. Upon the mucous and serous membranes small 
collections may be readily seen, and may present either a pseudo- 
membranous appearance or may appear as opaque plates upon or 
beneath the surface. Microscopically there are three chief sites : 




Fig. 15.— Cylindroma, showing a number of blood-vessels whose walls have become 
converted into hyaline material. 

(a) In the blood-vessels, where the degeneration may appear 
in the endothelium, beneath it, between the coats and fibers of 
the vessel, or surrounding the vessel. The wall is thickened, the 
lumen is narrowed or obliterated ; the endothelium may be in a 
state of proliferation. Perivascular hyaline change is well seen in 
certain tumors — cylindromata (Fig. 15). (b) In the interstitial 
tissues, as between the muscle-fibers, the hepatic cells, the renal 
tubules, in the reticulum of lymph-glands, in the retina, and in 
neoplasms and cicatrices. It may be uniform in distribution, but 
is more often irregularly clumped or may be in concentric whorls. 
In tuberculous foci the reticular fibrillar become swollen and gelat- 
inous in appearance. They may swell to such a degree that the 



78 



TEXT-BOOK OF PATHOLOGY. 



whole focus has a uniformly waxy appearance, the cells enclosed in 
the meshes meantime undergoing complete necrosis. In sclerosis, 
as in the liver, the newly-formed connective tissue may assume 
a hyaline character, the fibers being so closely packed together 
and transformed that the mass has a homogeneous appearance, 
(c) Within the cells. This condition is probably limited to meso- 
dermic cells. It may be seen in muscle- and giant-cells, and in 
endothelium, leukocytes, or wandering cells to a less degree. 
Whether the epithelial cells take part in this transformation in the 
coagulation-necrosis of mucous membranes and in the production 
of casts in nephritis has not been decided. It has not been pos- 
sible in the intercellular or interstitial varieties to decide whether 
the substance was formed there or deposited there ; in the vascular 
form, and especially in coagulation-necrosis and fibrinous exuda- 
tions, it is more probable that it is formed in loco. 

Unstained, the substance has a glistening, waxy appearance ; 
it is less translucent than amyloid. Typically it evinces an affin- 
ity for the acid anilin-stains. Stained with van Gieson's mixture 
of picric acid and acid fuchsin, the hyaline substance takes on a 
brilliant red color. It may or may not take the fibrin-stains ; it 
often takes basic stains in a modified manner. In truth, the 
reactions of hyaline material are very uncertain and shifting : in 
many instances it can scarcely be distinguished from amyloid, and 
the change is then called hyalo-amyJoid ; in other instances the 
product closely resembles mucin and the colloid substance. The 
cells of affected parts often show fatty degeneration or other alter- 
ations. 

Seats. — The locations most often affected are the muscles, espe- 
cially the recti, the mucous membranes, the liver, kidneys, and 
adrenal bodies, the cardiovascular system, the nervous system, the 
serous membranes, and the retina and choroid coats of the eye. 
The other locations are suggested in the discussion of the etiology. 

Pathologic Physiology. — Yon Recklinghausen believed it to 
be a coagulation of normal proteid upon the death of the cells ; 
this explanation is, however, insufficient. It appears more likelv 
either that it consists of proteid modified in loco by disturbed 
action of cells, or that it is a deposition by cellular carriers of 
insoluble material formed elsewhere. The exact nature of the 
transformation is entirely obscure ; it cannot be held analogous 
to the coagulation of proteids by heat ; nor to the precipitation by 
metals or salts, since in these events the proteids are not usually 
rendered permanently insoluble in water and are in other ways 
clearly different. Hyaline material can undoubtedly be recon- 
verted, absorbed, and removed. Its presence rarely compromises 
the parenchymatous structures to an extreme degree. It may be 
converted into the other albuminoid degenerations, and may un- 
dergo caseation and also calcareous infiltration. 



RETROGRESSIVE PROCESSES. 



79 



MUCOID DEGENERATION. 

Definition. — Theoretically this is the conversion of cellular 
protoplasm into mucin. Mucin is a glycoprotein which contains 
no phosphorus, and which by virtue of its carbohydrate moiety 
reduces cupric sulphate in alkaline solution. It is quite insoluble 
in water, but has itself a marked capacity for taking up water. It 
is very soluble in alkaline solutions, but is precipitated by satura- 
tion with most neutral salts. It is precipitated by acetic acid from 
solutions poor in salts ; also by heat, alcohol, and many of the 
metals. It does not dialyze. The secretions from different classes 
of epithelium differ notably among themselves, and the pathologic 
mucins differ still more. 

Etiology. — Mucoid transformation should be distinguished 
from hypersecretion of mucin. Hypersecretion is a common re- 
sult of inflammation or irritation of all sorts ; it is seen in the 
pulmonary, gastro-intestinal an # d urinary mucous membranes, in 
the glands of Cowper, the gall-bladder, the salivary glands, in the 
antrum of Highmore, in the lachrymal glands, and in the testicles. 
The product of the epithelium of the urinary tract and gall-blad- 
der, usually called mucin, is more often nucleo-albumin. Mucoid 
degeneration in the strict sense occurs most frequently in meso- 
blastic tissues, the abnormal substance lying between the cells. 
It is in some way connected with inflammatory processes, as, apart 
from its occurrence in tumors, it is found only in tissues the seat of 
inflammation. Any of the connective tissues of the body may be 
affected. Widespread myxomatous degeneration of the subcuta- 
neous tissues may be seen in myxedema. In some cases of myx- 
edema, scleroderma, and the other pachydermic affections, mucin 
has been extracted from the skin ; other attempts in similar cases 
have failed. Neoplasms comprise the third group of mucoid phe- 
nomena. The transformation occurs in sarcomata, carcinomata, fibro- 
mata, lipomata, chondromata, and especially in the myxomata, in 
which mucin is the essential element, while in the other growths 
it is an accidental and occasional transformation. In the epithelial 
tumors the epithelial cells themselves may be affected. 

Pathologic Anatomy. — The gross appearances may consist 
in nothing but the appearance of the mucin. Upon catarrhal 
mucous membranes is a coat of thick, tenacious mucus, with or 
without congestion or other changes. In localities where the 
mucin becomes pent up it swells markedly, dilates the chambers, 
flattens the epithelium (which may then atrophy), and later 
becomes converted into a simple albuminous fluid. Such a pro- 
cess is seen in the antrum of Highmore, in Cowper's glands, in 
the salivary glands, in the gall-bladder, in the vermiform appen- 
dix, etc. ; in these cases the appearances are those of a cyst. In 
mucoid degenerations in the connective tissues the appearances are 



80 



TEXT-BOOK OF PATHOLOGY. 



























































t ft 
























m- * *. -J* 






ft*""* V 

















often not characteristic of mucin ; the tissues are soft and elastic 
and tear easily. In tumors, cysts are usually formed along with 
general mucoid infiltration. In cystic ovarian neoplasms the pro- 
duction is often massive, and the substance is often peculiar in 
refusing precipitation by acetic acid, and has therefore been termed 
pseudomucin. , In myxomata the substance is usually much more 
dense. 

Microscopic Appearances. — In catarrhal mucous membranes 
the goblet-cells are seen in excessive quantity. Only in extreme 

instances is the process accompanied 
by the death of the cell. The cells 
are much swollen, and the distal 
end is especially bulged out with 
its drop of mucin. There is usually 
a submucous inflammatory reaction, 
and pus-cells containing mucoid ma- 
terial may be seen. In the con- 
nective tissues it is seen that the 
mucin lies between the cells and 
that the ground-substance has disap- 
peared — i. e.y been converted into 
mucus (Fig. 16). The cells very 
rarely present mucous change, but 
are often degenerated in other ways. 
In tumors the change may occur in 
and between the cells and in the 
of cysts, whose walls may or may not present a cellular 
lining. The blood-vessels are rarely affected. In all situations 
mast-cells may be seen, often abundantly. 

Mucin is best fixed with corrosive sublimate. As a rule, it 
elects basic stains. It stains only moderately with hematoxylin, 
but very well with methylene-blue and indeed with most of the 
basic anilin-stains. Thionin and tuloidin-blue are the best stains, 
giving it a purple-red color. These staining reactions are not en- 
tirely distinctive, and it is often impossible to differentiate mucoid 
from colloid material, and even from hyaline and amyloid material. 

Seats. — Of normal epithelial tissues the mucosa of the respi- 
ratory and gastro-intestmal tracts, the salivary glands, and the 
uterus are most often affected ; any epithelium may, however, be 
involved. The connective tissues have been sufficiently consid- 
ered. Of neoplasms, ovarian cysts, abdominal carcinomata, and 
mesoblastic tumors anywhere are most liable. 

Pathologic Physiology. — Since the deposition of mucin 
seems to be excluded, the only explanation is to assume the con- 
version of other proteids into mucin. The causes and modus 
operandi are not clear ; the fact, however, that in the cysts the 



Fig. 16.— Myxomatous degeneration 
of a sarcoma, showing stellate cells 
separated by mucoid intercellular ma- 
terial (Karg'and Schmorl). 



form 



RETROGRESSIVE PROCESSES. 



81 



mucin may be reduced to simple albumin, shows the possibility 
of such transformations. 

Unless the disease is very prolonged, affected mucous mem- 
branes may recover. The connective-tissue forms do not of them- 
selves threaten the life of the tissue ; and the deposit is often 
removed by reabsorption. In neoplasms the degeneration seems 
an evidence of cell-death. 



COLLOID DEGENERATION. 

Definition. — This consists in the abnormal appearance of a 
substance whose prototype is the colloid material of the thyroid 
gland. It is not precipitated by acetic acid nor alcohol, does not 
take up water avidly, and is therefore much like the pseudomucin 
already noted. 

Etiology. — It occurs in goiters and in thyroid neoplasms, in 
the hypophysis cerebri, in the kidneys (some cases of congenital 
cysts), and the adrenal bodies, in the prostate and seminal vesicles, 
in the atrophic gastric mucosa, in cysts of the lips and larynx, and 
in the cervix uteri. Colloid transformation in neoplasms apart 

































Ft ' ¥ ; 



Fig. 17.— Colloid degeneration of the thyroid gland, showing masses of colloid matter in 
the gland acini (Karg and Schmorl). 

from those of the thyroid body is very rare. Colloid may arise 
from or become converted into mucoid material, and stands very 
close to the hyaline substance. 

Pathologic Anatomy. — Affected organs maybe enlarged, and 
may be hard or quite soft. On section the colloid areas appear as 
yellowish-brown translucent bodies ; rarely they are arranged in 
large clumps. They may be macroscopically invisible, or, on the 
6 



82 



TEXT-BOOK OF PATHOLOGY. 



contrary, may form large cystic collections with thin, flattened 
walls. Colloid degeneration may be accompanied by serous trans- 
udation, due probably to vascular disturbances. The serous trans- 
udation seems to dissolve the colloid material, so that finally the 
cysts form compartments filled with a chocolate-colored fluid con- 
taining pus, blood, and crystals of cholesterin, sodium chlorid, 
and calcium oxalate (Fig. 17). 

Microscopically the material is found in the glandular acini, in 
the cells, and in the connective tissues. There are often signs of 
pressure, and, probably from the same cause, the areas are ane- 
mic and have a poor vascular supply. The arrangement is 
usually in balls or whorls, homogeneous as a rule, but often with 
concentric or radiating lines. The areas often intercommunicate, 
and extensions may be traced into the adjacent tissues. The cells 
usually show degenerative changes, and inflammatory reactions 
are often present. Crystals of calcium oxalate are common. Acid 
stains are usually elected, as in hyaline degeneration. The indefi- 
niteness of the reactions may make it impossible to exclude hya- 
line and mucoid changes. 

Pathologic Physiology. — This is obscure, but seems to be 
analogous to that of mucoid change. The substance is undoubt- 
edly produced in loco. 

Colloid is a grave degeneration, usually connected with marked 
cellular disturbances. The substance may become hyaline or mu- 
coid, or may be replaced by a simple or purulent exudation. 

GLYCOGENIC INFILTRATION. 

Definition. — This condition consists in the presence of gly- 
cogen in cells which normally contain none, or the presence of an 
excess in cells which normally contain it, as in the liver, cartilage, 
muscles, leukocytes, in the embryo in all tissues, and in the uterus. 
The attempt has been made to separate glycogenic infiltration 
from a glycogenic degeneration, but the conversion of protoplasmic 
proteid into glycogen has never been demonstrated. 

Etiology. — The condition is not infrequent. It is seen in the 
tissues in diabetes, especially in the kidneys, muscles, liver, and 
circulating leukocytes. It occurs in neoplasms, especially in 
malignant growths of mesoblastic origin, being rare in most carci- 
nomata. In leukocytosis of different varieties the cells may con- 
tain an excess, and granules of the glycogen may float free in the 
plasma. In purulent collections and in inflammatory areas the 
cells may be markedly infiltrated. The infectious granulomata, 
however, seem exempt. The amylaceous bodies of the prostate 
are closely allied to glycogen. 

Pathologic Anatomy. — Tissues rich in glycogen may pre- 
sent a hyaline appearance ; usually there are no macroscopic alter- 



RETROGRESSIVE PROCESSES. 83 

ations. Microscopically the material is generally found within 
the cells ; it may, however, be in the intercellular substance, and 
may be free in the plasma of blood or the fluid of exudates. It 
is commonly deposited as round balls, which may be concentri- 
cally striated. In fresh tissues it is soluble in water, but loses its 
solubility after fixation by alcohol, etc. 

Glycogen is stained brown by iodin, but the brown is not 
turned blue on the application of sulphuric acid. Ptyalin or amyl- 
opsin converts it into sugar, with the loss of the color-reaction. 

The pathologic physiology is obscure. In diabetes it is 
simply an expression of the general hyperglycemia. In neoplasms 
and suppurations the collections are probably depositions. 

DROPSICAL INFILTRATION. 

By dropsical infiltration is meant edema of the cells, the pres- 
ence in cells of an excess of plasma. This does not always occur 




Fig. 18.— Dropsical infiltration of the epithelial cells of a carcinoma of the breast : a } 
ordinary epithelial cells; b, dropsical cells; c, dropsical nuclei; d, enlarged nucleoli 
(Ziegler). . - 

in general dropsy, the fluid being between the cells and often 
compressing them to a marked degree. In other instances the 
cells take up the fluid. In burns and pemphigus and in other 
skin-lesions connected with vesiculation, and in various inflamma- 
tions of organs, edema of the cells occurs. It is also a part of the 
degeneration termed cloudy swelling. 

The cells are enlarged, often to an extreme degree, and they 
may even burst. The protoplasm sooner or later becomes cloudy 
and often presents degenerative changes — fatty metamorphosis in 
particular. Vacuolation is frequently observed (Fig. 18). 

The condition is probably a purely physical phenomenon in the 
dropsies. In the cutaneous lesions other factors are operative. 



84 



TEXT-BOOK OF PATHOLOGY. 



CALCIFICATION. 

Definition. — Calcification consists in the abnormal deposition 
in tissues of earthy salts. The phosphates and carbonates of cal- 
cium are the chief salts concerned, the oxalates, however, are often 
present ; and the corresponding magnesium salts may be mixed 
with them. The best physiologic examples are the senile change 
in the vascular apparatus and the formation of the brain-sand 
(acervulus cerebri). Calcification of the skeletal tissues is usually 
accomplished as a physiologic process through the activities of 
special cells ; this is an essential element in ossification. 

Etiology. — The deposition generally occurs in diseased tis- 
sues, especially in those the seat of vascular disorders. Local 
necrosis or fibrosis antedates intercellular calcification, and the 
process may be accompanied by atrophy and absorption of certain 
cellular elements. In neoplasms abnormal cellular conditions 
certainly predispose ; but here, too, the vascular relations are of 
notable importance. Hyaline and fatty degenerations often pre- 
cede or accompany calcification. 

In rare instances no local predispositions can be determined. 
Cases of this kind occur in old age, and in these cases it is inferred 
that, owing to increased lime-resorption from the skeleton, the 
system is saturated to the point of precipitation (metastatic calci- 
fication). Similar supersaturation of the blood with calcareous 
matter may occur in cases of extensive disease of bones, and may 
lead to widespread deposition. 

Pathologic Anatomy. — Early in the process no macroscopic 
signs are apparent. On microscopic examination the salts are seen 
as fine granules scattered through the intercellular substance. Cell- 
ular infiltration, however, is not uncommon, and in such instances 
the cells show more or less extensive nuclear and protoplasmic 
degenerations. By the coalescence of the granules larger, irregu- 
larly spherical bodies may be formed. These usually have a con- 
centric arrangement (psammoma bodies). Definite crystals are rare, 
but may be seen. The next adjacent tissue may present an opaque 
appearance. In certain localities, especially the blood-vessels and 
serous membranes, calcareous plates are formed. The depositions 
may attain a surprising size, especially in the vessels and in neo- 
plasms. The color of the deposits is usually white, grayish, or 
yellow ; accidental pigments may, however, produce discolorations. 
On staining the deposition takes up both carmine and hematoxy- 
lin, but exhibits no elective attraction for the anilin dyes. The 
salts are dissolved by acids, best by hydrochloric acid ; in the case 
of carbonates, with evolution of carbonic acid gas. Many organic 
and inorganic acids are employed in the decalcification of tissues 
for purposes of microscopic study. Fibrosis, cellular necroses, 
and degenerations can be demonstrated in the tissues by suitable 
methods. 



RETROGRESSIVE PROCESSES. 



85 



Seats. — It is in the cardiovascular system that the condition is 
of the most importance. It often occurs as a simple senile change, 
usually connected with an atrophy of the elastic tissues of the 
vessel-walls, hyaline degeneration of the connective tissue, and 
general fibrosis. It is almost invariably an accompaniment of 
sclerotic endocarditis and arteriosclerosis. In the endocardium the 
valves are most frequently affected ; of the vessels, the aorta, the 
coronary arteries, and the cerebral vessels. The process is, how- 
ever, often universal, and the splanchnic vessels and radial arteries 
seem very susceptible. It affects chiefly the intima and media. In 
the pericardium the deposition is uncommon without the previous 
occurrence of pericarditis ; in adherent pericardium the heart may 
be literally enclosed in a calcified sac. In the myocardium calci- 
fication is usually interfibrillar, but may involve the fibers. Large 
collections may occur in the pituitary body, the meninges, and in 
the ventricular plexuses. It is c*ommon in the joints, uncommon 
in the pleura, rare in the peritoneum. In the muscles local for- 
mations are not rare, and usually occur at the seat of previous in- 
jury or irritation. In the lungs and liver it is not unusual in and 
around foci of necrosis due to various causes (tuberculosis, parasites, 
etc.). Cicatricial tissue often becomes calcified. In the walls of 
cysts, in the biliary and urinary bladders, in the limiting wall of 
old abscesses and hematomata, in thromboses, and even in cutaneous 
scars calcification is a common incident. In the kidneys infarcts 
of these salts may be formed. The neoplasms most subject are 
the avascular tumors : uterine fibromata, fibromata in general, der- 
moid cysts, goiters, scirrhous carcinomata, tumors of the pituitary 
bodies, and especially neoplasms involving bones or cartilages. 
It may, however, occur in the most vascular sarcomata. The 
special term psammoma (q. v.) is applied to certain calcified 
neoplasms. Lithopedia are the calcified fetuses of extra-uterine 
pregnancy. Apart from neoplasms, the most striking intracellular 
depositions are seen in the ganglion-cells in areas of softening and 
in the renal cells following certain metallic poisonings (mercury). 
It is interesting to note that the intestinal epithelium, which 
normally secretes the larger part of the lime-salts discharged from 
the body, is rarely infiltrated by them. 

Pathologic Physiology. — Various views are held to ex- 
plain the depositions. An excess of the salts in the blood or tissue- 
liquids must be rare. On the one hand, it has been assumed that 
the soluble are converted into insoluble salts, and, on the other 
hand, that the tissues have become less solvent for the salts. 
Probably the best established view is that the salts are precipi- 
tated as insoluble combinations with proteids. 

Calcareous deposits are probably never removed, but once 
formed remain permanently. There is no doubt that they in- 
fluence the adjacent tissues, causing degenerations. 



86 



TEXT-BOOK OF PATHOLOGY. 



OSSIFICATION. 

Ossification implies the deposition of lime-salts and other changes 
through the agency of osteoblastic cells. It occurs in cartilages, and in 
tumors connected with the bones, cartilages, and periosteum. The salts are 
regularly deposited and are usually in masses between the cells. An 
accurate differentiation from calcification can in some instances be made 
only by the detection of osteoblasts after decalcification of the material. 



URATIC INFILTRATION. 

Deposits of urate of sodium in the cartilages and fibrous tissues of joints 
and in various other situations occur in the course of gout (see Disturbances 
of Metabolism and Diseases of Joints). 

PIGMENTATION. 

According to the origin and variety of the pigments, pigmenta- 
tions may be divided into four groups : 1, those in which the pig- 
ments are derived from external sources ; 2, those derived from 
the hemoglobin ; 3, those derived from the bile ; 4, those derived 
from cellular activity within the organism. 

Pigmentation from the Exterior. 

Of the first group, those caused by entrance of foreign bodies 
through the air-passages are the most important. The condition 
now generally termed pneumonokoniosis is commonly a disease 
of occupation. Coal, iron, and stone are the most frequent foreign 
substances inhaled. Vegetable particles, as grain-dust and textile 
fibers, and animal hairs and furs are not uncommonly the cause of 
such pigmentations. Corresponding to the agent, there are such 
terms as anthracosis (coal-dust pigmentation), siderosis (iron), cal- 
cicosis (stone), etc. (Fig. 19). Inhaled substances probably do not 
reach the alveoli, but are caught by the bronchial cellular cilia. 
In part they are coughed up or otherwise cast on° with the bron- 
chial secretions ; in part they penetrate the bronchial walls or are 
carried by phagocytic cells into the submucosa (Fig. 20). They 
may become deposited in the latter situation, or may be carried in 
the lymphatic circulation to the peribronchial and mediastinal 
glands, the fibrous tissue of the lung, or the subpleural tissues. In 
rare instances the pigment finally reaches the general circulation, 
following which it is deposited largely in the spleen, liver, intes- 
tinal mucosa, and kidneys. In these cases the mucous membranes 
from the lips downward may be more or less pigmented. 

Pigmentation through the alimentary tract is best illustrated by 
argyria following the excessive ingestion of soluble salts of 
silver. The depositions seem to consist of a reduced form of a 



RETR GRESSIVE PR OCESSES. 



87 




Fig. 19.— Tuberculosis of the lung, showing anthracotic pigmentations in the lower part. 

silver albuminate. In the skin the pigment lies directly under the 
epithelial layer, between the cells, and in the intercellular tissue 




Fig. 20.— Phagocytic cells of the bronchial secretion (sputum) containing black particles 
of dust and carbon ; the cells on the right are stained with methylene-blue (Jakob). 

and lymph-spaces. The gastric and intestinal walls are deeply 
affected. The liver and kidneys are usually involved ; in the 
former the deposition is periportal, in the latter the glomeruli and 



88 



TEXT-BOOK OF PATHOLOGY. 



the corticomedullary boundary contain the pigment ; in both the 
cells are free. Among the rarer sites are the choroid plexus, the 
various glands of the body, and the Avails of the blood-vessels. 

Pigmentation by cutaneous absorption apart from tattooing is 
problematical ; it has been alleged to occur in workers in copper. 

Hematogenous Pigmentation. 

This concerns the deposition of pigments derived from the 
hemoglobin, of which there are two groups, the siderous and the 
non-siderous. The chief siderous pigment is hemosiderin, which 
has, however, many modifications ; the non-siderous pigments are 
derivatives of hematin — hematoidin, hemofuscin, melanin, etc. 
In the course of time the siderous pigments may lose their iron. 
Probably all formation and further elaboration of these pigments 
are the result of specific cellular activities. Two groups of hema- 
togenous pigmentations may be distinguished, (1) those in which 
the hemolytic agents act in the circulating blood or the associated 
organs, and (2) those in which the reductions occur in local tissues. 

(1) To the first group belong the general hemolyses. In per- 
nicious anemia and leukemia, in malaria, in severe cachexias, in 
occasional infectious and septic processes, in poisonings (as by pyro- 
gallic acid, chlorates, arseniuretted hydrogen, by some mollusks, 
by pyridin and tuluylendiamin, etc.), the hemoglobin is set free in 
the circulation. It is promptly excreted by the kidneys, and to a 
limited extent by the intestines ; much is converted into bile in 
the liver, some little passing into the bile unchanged. A certain 
amount is reduced by the tissues (apparently by the liver) to the 
two before-mentioned series of pigments, which are then carried in 
the lymphatic and vascular circulation and by means of cellular 
carriers and deposited in various places. As time passes, these 
pigments seem to become reduced, the iron being excreted by the 
intestine and the remainder by the kidneys as urobilin. In the 
liver the depositions are largely in the periphery of the lobule ; in 
the spleen, in the regions of the follicles ; in the kidney the most 
marked collections are in and about the glomeruli and the tubules. 
In all tissues the depositions are both intercellular and intracellu- 
lar ; the cells may either take up pigment or have it deposited in 
them. 

A peculiar form of hematogenous pigmentation (hemochro- 
matosis) is that seen in the gastro-intestinal tract and other ab- 
dominal organs of drunkards and in cachectic conditions. In other 
instances the presence of siderous pigments in the intestine is to 
be viewed as a process of excretion, since the greater mass of iron 
is eliminated through the bowels. A form of widespread hemo- 
chromatosis with hypertrophic cirrhosis of the liver and glycosuria 
has been described under the name diabUe bronzL 



BETE OEESSIVE PROCESSES. 



89 



The appearance of organs with marked pigmentation varies 
with the variety and stage. A rusty-red color is the usual early 
appearance ; later a brown, then a greenish color may be produced, 
and finally a dark blackish-brown. The association of jaundice, 
which is common, alters appearances very much. 




Fig. 21.— Phagocytic cells of the sputum containing blood-pigment, from a case of cardiac 
congestion of the lungs (Jakob). 

(2) The two chief causes of local pigmentation are thrombosis and 
interstitial hemorrhage and coagulation. The pigmentations seen 
in the indurations resulting from prolonged venous stagnations and 
congestions are probably of analogous origin. Under these cir- 




Fig. 22.— Hematoidin-crystals from an old hemorrhagic focus (Jakob). 

cumstances the hemoglobin is diffused from the blood-cells, and a 
portion passes directly into the plasmatic circulation and is carried 
away to be eliminated ; soon, however, the area becomes walled 
olf and the two sets of pigments are then formed within. The 
siderous pigments are most frequently seen in small lesions and at 



90 



TEXT-BOOK OF PATHOLOGY. 



the periphery of large ecchymoses ; the hematoidin series is most 
prevalent within the cystic contents. The pigments change in 
color (the color-changes in a bruise are due to this), and finally 
become a brownish amorphous matter, which in turn disappears. 
Phagocytic cells take up all forms of the pigments (Fig. 21), and 
carry them to various parts of the body, especially to the liver, 
hematopoietic organs, intestines, and glands ; the depositions in 
them are known as pigment-metastases. 

The distinctive reactions of the various pigments are not well 
known. Of hematin and hemin it is known that they are insolu- 
ble in water, alcohol, and ether ; slightly soluble in weak acetic 
and mineral acids ; easily soluble in chloroform and in weak alka- 
lies, from which solution they are precipitated on the addition of 
lime- or baryta-water. Hematoidin differs from these in being 
somewhat soluble in ether, but insoluble in weak acetic acid, and 
gives with strong nitric acid the spectral play of colors. Apart 
from the iron reactions little is known of hemosiderin. The iron 
is best demonstrated by its conversion into the sulphid by means 
of ammonium sulphid, or by the Prussian-blue reaction with weak 
hydrochloric acid and potassium ferrocyanid. 

Microscopically hematogenous pigment presents three chief 
appearances : small needles, rhombic crystals, and amorphous 
masses or fine balls clumped together (Fig. 22). The first two 
forms are very rarely seen within cells, the last form commonly. 
The colors vary from a pink-red to a deep rubin, from pale yellow- 
green to a deep brown or absolute black. 

Hepatogenous Pigmentation. 

Pigmentations derived from the bile are due to bilirubin (iso- 
meric with hematoidin) and its oxidation-product, biliverdin. As 
will be elsewhere explained in detail, all jaundice is now held to 
be of hepatic origin ; so far as known, only the hepatic and renal 
cells can produce bilirubin from hematin. 

The deposition of these pigments may be either in solution in 
the tissues, in granular precipitations, or in crystals (needles and 
rhombic plates). The cerebral substance alone seems never, ex- 
cept in the new-born, to be pigmented. The liver, skin, mucous 
membranes, the endarterium and other serous membranes, and the 
glandular and fatty tissues are especially susceptible. The color^ 
is first yellow and gradually deepens to a deep olive, the urine 
presenting similar transitions. The lachrymal and salivary glands, 
the mammse, and the intestinal mucosa seem to be able to keep the 
pigment from passing out with their secretions. The ocular fluids 
are colored. 

The pigment in solution saturates the tissues. The granular 
pigments, yellow, brown, or greenish in color, may be seen in the 



RETROGRESSIVE PROCESSES. 



91 



cells or in the interstitial tissues ; the crystals, yellow or red in 
color, are usually extracellular. The pigment displays the spec- 
tral play of colors on contact with strong nitric acid, and is turned 
green by weak tincture of iodin. 

A special form of deposition is the bilirubin-infarct in the uri- 
nary tubules. These are seen in severe jaundice of the new-born, 
but may occur in deep icterus of adults, as in acute yellow atrophy. 

Metabolic Pigmentation. 

The pigmentation derived from cellular activity may be prop- 
erly termed metabolic. We know isolated facts about the differ- 
ent forms, but there is little systematic fundamental knowledge. 
Two facts, however, seem clear : that these pigments are formed 
by migratory and resident pigment-building cells, which with 
leukocytes and plasma-cells accomplish the transportation and 
deposition of the pigments ; and that hemoglobin is in some way 
or other the raw material for their manufacture, with, perhaps, 
the exception of some pigments in melanosarcoma, which seem 
derived from proteids. 

The manifestations may be local or general. Among the former 
are the pigmentations of nevi and moles, of pregnancy, of the 
corpus luteum, freckles, some scars, certain skin-diseases, as chlo- 
asma and xanthelasma, of the lesions secondary to some cutaneous 
parasites, etc. A special local type is that seen in tumors, notably 
in melanosarcomata. Lipomata and sarcomata (chloromata) may 
be analogously affected. 

Among the general pigmentations are those of Addison's disease, 
of certain severe anemias and cachexias, of tuberculosis of the 
peritoneum, intestines, and retroperitoneal glands, of abdominal 
neoplasms, and of senility. The cases associated with abdominal 
lesions are held to be connected with disturbances of the adrenal 
bodies or of the splanchnic sympathetic system, which has been 
considered to have control of pigment-formations. 

The metabolic pigments are very varied, and a detailed discus- 
sion of them here would be unprofitable. They may have a high 
percentage of sulphur, and may or may not contain iron. They 
are commonly deposited in and between the cells as granules, but 
may be crystalline. They do not give a play of colors with nitric 
acid, and have varying solubility. 

NECROSIS. 

Definition. — Necrosis may be defined as the death of tissues. 
The death of individual cells is termed necrobiosis ; death of tissue 
en masse, usually accompanied by putrefactive changes, constitutes 
gangrene. 



92 



TEXT-BOOK OF PATHOLOGY. 



Etiology. — All classes of cellular death may be brought un- 
der four etiologic groups : 1, those due to nutritional and circula- 
tory disturbances ; 2, those due to trophic disturbances ; 3, those 
due to poisons — animal, vegetable, bacterial, and inorganic ; and, 
4, those due to traumatism, employing the term in its broadest 
sense. It has been attempted, without success in our opinion, to 
class the trophic necroses as identical with those due to circulatory 
and nutritional disturbances ; similarly the poisons and traumatism 
have been considered as acting only through the circulatory and 
nutritional paths, but it seems evident that in the light of our 
present knowledge the four groups are to a greater or less degree 
distinct. 

The various causes do not produce constant types of necrosis, 
but occasion one form in some cases, another in other cases. Prom- 
inent among these varying circumstances are the native health of 
the tissues and their vital resistance, the circulatory relations of the 
part involved, the activity and duration of the causal agents, the 
age of the subject, the presence of other diseases, the temperature 
of the tissues, etc. It will therefore be better first to consider col- 
lectively the causes of necrosis, and subsequently detail the varieties 
of it. There can be no doubt, however, that in the direct forms 
of necrosis the results are to a marked extent individual to the 
agent ; for example, cells killed by the action of acids, alkalies, 
and metallic salts present appearances quite characteristic of 
each. 

Circulatory Derangements. — The circulatory disturbances in- 
clude many conditions. Acute and chronic ischemia, however 
produced — by embolism, thrombosis, arteriosclerosis and atheroma, 
by extra-arterial pressure, by cardiac weakness, or by arterial 
spasm, as in Raynaud's disease and perhaps in ergotism — are im- 
portant conditions. Venous stagnations are responsible for many 
instances. Actual stasis due to mechanical obstructions and such 
poisonings as produce coagulations is a rare cause. Heat and 
cold act partly by circulatory disturbances. Among the general 
disorders of circulation and nutrition may be mentioned the 
anemias, the cachexias, senility, and certain metabolic diseases, 
such as diabetes. In these conditions there is much probability 
that poisoning by metabolic products plays an important part. 

Trophic Derangements. — Forms of necrosis due to trophic dis^ 
turbances are well illustrated by bedsores (decubitus), myelitic 
cystitis, the ulcerations seen in trigeminal neuritis, and the 
arthropathies. These forms of cell-death cannot be brought under 
the circulatory, toxic, or traumatic classification. They can be 
explained only by the assumption that the biologic mechanism of 
the cell is disturbed, and that in consequence death occurs. 

Intoxications. — The group due to poisons is very extensive 
and the particular subdivisions numerous. The toxins of bacteria 



RETROGRESSIVE PROCESSES. 



93 



furnish many examples of direct necrosis, and act indirectly in 
cases which seem circulatory or traumatic, though they are not 
really so, since these factors only lower the resistance of tissues, 
which then become susceptible to bacterial infection. Experi- 
mentally the most exquisite forms of cell-degenerations and necrosis 
can be produced by the injection of toxins or analogous substances 
like ricin and abrin. The alkaloids possess marked power in the 
production of necrosis. Acids, alkalies, metallic salts, and innumer- 
able other chemical substances may produce direct necrosis, or indi- 
rect necrosis by the preliminary production of degenerations. The 
same substances often cause both circulatory and mechanical dis- 
turbances, which augment their direct effects. Heat and cold act 
like chemicals ; heat alters the properties of proteids ; cold affects 
the fluids rather than the protoplasmic substances ; both also 
induce marked circulatory disturbances. 

Mechanical Agents. — The mechanical causes of necrosis are 
many and varied. Pressure per se may cause the death of cells, 
but is often aided by the circulatory disturbances which it occa- 
sions. That tension causes necrosis is an old surgical truth, well 
illustrated by the results of collections of exudates below the peri- 
osteum and by the results of strangulations. The pressure of cal- 
culi, concretions, enteroliths, and exostoses may cause important 
necrotic processes. Circulatory disturbances often are a very ac- 
tive factor — indeed, many forms of traumatism act solely through 
them. 

Inflammation, whatever its original inception, may become so 
extreme as to lead to necrosis. Necrosis, on the other hand, often 
leads to inflammation, the dead cells constituting the primary irri- 
tants. 

All forms of necrosis are accompanied to a greater or less 
extent by the various degenerations. In particular the cellular 
alterations are constantly present, and constitute the evidences of 
morbific action. (Reference will be made below to the cellular 
changes.) 

There are several general forms of necrosis which, however 
produced, have a sufficiently distinct character to warrant separate 
descriptions. They are coagulation-necrosis, liquefaction-necrosis, 
caseation, fat-necrosis, hemolysis, and gangrene. 

COAGULATION=NECROSIS. 

Definition. — This is defined as that form of death of tissue 
in which the proteid suffers a change similar to or identical with 
coagulation. It is seen only in those tissues which are rich in 
proteids. The process is partly at least a species of fibrin-forma- 
tion, and is allied to hyaline degeneration. 

Etiology. — The causes of this condition are those above de- 



94 



TEXT-BOOK OF PATHOLOGY. 



tailed for necrosis in general. Circulatory disturbances, except 
thrombosis or infarctions, play a minor rdle here. Chemical irri- 
tants and high temperatures frequently produce it. Bacterial 
poisons are very prone to produce it, especially those elaborated 
by the pyogenic bacteria, the tubercle bacillus, and the Bacillus 
diphtherial About every abscess is found more or less coagula- 
tion-necrosis ; it is one of the early changes in tubercles, and the 
fundamental element in the production of pseudomembranes. All 
exudates and transudates are liable to coagulation. 

The serous and mucous membranes are most susceptible ; next 
the muscular tissues (often the myocardium). 

Pathologic Anatomy. — The tissue has a glazed, opaque, 
waxy appearance, and is firmer and paler than normal. In later 
stages the color becomes gray and the tissue inclines to soften. 
Microscopically it is seen that there is an exudate which has been 




Fig. 23 —Obstruction of a branch of the renal artery with micro-organisms : necrosis 
of the tissue around the arterv, and round-cell infiltration of the neighboring tissue 
(Thoma). 

fixed in the tissues ; fibrin is seen (with suitable stains) in the 
form of granules and fibrils. In addition to the fibrin there is 
more or less homogeneous matter (fibrinoid) which does not react 
to stains like fibrin, but which is nevertheless closely allied to that 
substance. The cells soon lose their election for stains (Fig. 23). 
Early in the process the nuclei may stain faintly and present a 
homogeneous appearance ; later the cell disintegrates completely 
(Fig. 24). In muscles the stria tions disappear ; and in the car- 
diac muscle the intercellular cement-substance seems to be dis- 
solved, for the cells often lie separated and present vacuolation 
and fragmentation. Pus, leukocytes, and red blood-cells in the 
affected areas all suffer the fate of the fixed tissue. The blood- 



RETROGRESSIVE PROCESSES. 



95 



vessels at the margin of the area are seen to be thrombosed. In 
the kidneys the tubules may contain firm casts. 

Morbid Physiology. — Many chemicals cause coagulation by 
direct action. In the larger number of instances, however, it 
must be assumed that the fibrinogenetic substances which bring 
about the coagulation of the proteids are derived from the necro- 
biotic cells in the area or are carried thither by the lymphatic 




Fig. 24.— Coagulation-necrosis of the hepatic cells in a case of puerperal eclampsia 
(Karg and Schmorl). 

I 

cells. There is considerable evidence that bacterial products may 
act fibrinogenetically. It has been contended that coagulation 
necrosis is simply a species of inspissation of the tissues. This 
is certainly not the case. 

An area of coagulation may be cast off by the process of ulcer- 
ation, may undergo liquefaction, caseation, or suppuration, may be 
encysted, and apparently may be dissolved and reabsorbed. The 
area of disease may finally be converted into scar-tissue by 
secondary regeneration. More or less complete loss of function 
results from this form of necrosis. 

LIQUEFACTION=NECROSIS. 

Definition. — This change consists in the death of tissue with 
colliquation. It may be divided into primary and secondary 
forms. Secondary liquefaction-necrosis is the form in which other 
varieties of necrosis or degeneration are followed by liquefaction. 
Thus, areas of coagulation-necrosis, cheesy necrosis, and of inflam- 
mation, gangrenous tissue, and tumors may become liquefied. 

Among the special forms may be mentioned vesicle-formation 
and the softening of caseous tuberculous lesions. A very frequent 
seat of liquefaction-necrosis is the central nervous system, where 
the conditions are unfavorable to coagulation, so that liquefaction 
here follows pathologic conditions which would elsewhere produce 



96 



TEXT-BOOK OF PATHOLOGY. 



coagulation. Circulatory disturbances, traumatism, and intoxica- 
tions all cause softening in the central nervous system ; the 
peripheral nerves are much less susceptible. 

Pathologic Anatomy. — In the early stages the tissue is 
softer than normal and very rich in juices. Later, when the solu- 
tion of the fibrillar tissues is advanced, the area becomes filled 
with a liquid of greater or less consistency, depending upon the 
tissue involved. The cells in the area are seen in all stages of 
degeneration ; later, nothing but detritus is visible. In some 
instances, instead of becoming more and more fluid, the exudate 
undergoes coagulation. The color may be white, from the presence 
of an emulsion of fats ; yellow, from fats and pigments ; red and 
brown, from the presence of blood-pigment ; and deeply colored 
when jaundice is associated. 

The process consists in the infiltration of fluid into tissues and 
the more or less complete solution of the tissue-elements in it. 
It has been compared to the alterations of proteids by digestion — 
a reasonable deduction, since enzymes are 
often elaborated in the processes which give 
rise to liquefaction. In other respects the 
process resembles the solution in distilled 
water of proteids precipitated by salt so- 
lutions. 

Areas of liquefaction may discharge 
their contents, may coagulate, may be re- 
absorbed, encysted, or in uncommon in- 
stances organized. 

CASEATION. 

Caseation is the crude name applied to 
a complex process whose product has a 
cheese-like appearance (Fig. 25). 

The condition is most frequently seen 
in connection with tuberculosis, although 
it is found in the other granulomata, and 
also in other pathologic processes. The 
fig. 25.— Tuberculosis of the preliminary conditio sine qua non of casea- 




suprarenal capsule, showing , 

caseation of the tuberculoul tlOn IS COagulatlOn-necrOSlS. 

RumVeT)° difiedfromKastand The early tubercle, before the occur- 
rence of softening, has an appearance like 
that of cheese, but is less homogeneous and more granular (Fig. 
26). A form of caseation quite similar in appearance occurs in 
pneumonia, in tumors, and especially in syphilis. Soft caseation 
is usually coagulation-necrosis advanced to liquefaction, together 
with fatty metamorphosis, so that the appearances are those of 
soft, creamy cheese. The liquefaction-necrosis of the central ner- 
vous system may present similar appearances. 



RETROGRESSIVE PROCESSES. 



97 



Microscopically, the tissues in caseation show no cells preserv- 
ing their staining-reactions ; everything is converted into debris. 
Around the affected area is usually found a zone of coagulation, of 
inflammation, or both. 




Fig. 26— Large tubercle of the lung, showing cheesy necrosis in the center. 

Tissues that have undergone caseation may be cast off, reab- 
sorbed, or encysted ; resolution is not possible. Calcification is a 
frequent termination. 

FAT=NECROSIS. 

This term is now used to designate a peculiar type of necrosis 
to which the fatty tissues are subject, and is distinct from ordinary 
fatty metamorphosis. In human beings it is seen almost exclu- 
sively in the abdomen, abdominal Avails, and subperitoneal fat. 
In nearly all instances it appears in connection with pancreatic 
disease — cysts, tumors, obstruction to the duct, and the various 
forms of acute pancreatitis. In rare instances the pancreas has 
not seemed especially diseased. In one case I have seen of hyper- 
trophic cirrhosis of the liver the omentum was affected, while the 
pancreas showed nothing but a moderate degree of fibrosis. 

The affected areas are white in color, usually not larger than a 
pea ; they may be soft or quite gritty. Inflammatory reaction 
may or may not surround them. On microscopic examination 
crystals of the fatty acids may be seen together with more abun- 
dant crystals of a combination of lime with the fatty acids. This 
combination, it appears, is not a primary feature in the necrosis, 
suggesting that the fatty acids are first set free and then unite 
with lime-salts. In experimental work by Hildebrand, Williams, 
and Flexner it seems to have been shown that the typical condi- 
tion may be the result of direct action of the fat-splitting ferment 

7 



98 



TEXT-BOOK OF PATHOLOGY. 



of the pancreatic secretion. It is certain, however, that in some 
cases of pancreatic cysts containing steapsin no fat-necrosis has 
occurred. Bacteria have been supposed by some to be the essen- 
tial agents causing the change, but this has not been demonstrated. 

HEMOLYSIS. 

Hemolysis, or blood-destruction, is a term limited to the red 
cells, and indicates destruction of the cell with dispersion of its 
hemoglobin. (The causes and other features are described under 
Pigmentations and Diseases of the Blood.) 

GANGRENE. 

Definition. — Gangrene, formerly defined as the death of tis- 
sue en masse, is perhaps best defined as the putrefaction of areas 
of necrosis. It may be 'primary, when a particular bacterium 
produces a gangrenous inflammation as its direct result, as in 
malignant edema ; or secondary, when saprophytic bacteria decom- 
pose an area already necrosed from other causes. It may be dry 
or moist, according to the location and supply of fluids. It may 
furthermore be circumscribed, progressive, or metastatic. 

Primary gangrene constitutes a specific affection, or rather a 
number of specific affections. Malignant edema, infectious em- 
physema, and some forms of anthrax may be included in this 
group. In these conditions there is violent infective inflammation 
with practically immediate gangrene of the affected parts. 

Secondary gangrene is more common, and the appearances are very 
varied. The essential condition is putrefaction of a necrosed area. 

Dry gangrene is usually due to vascular disturbances. As a 
result of arterial obstruction it is seen in the extremities in senility, 
and following arterial embolism or thrombosis of whatsoever nature 
if the collateral circulation be insufficient to nourish the part. 
Freezing may produce a dry form of gangrene, the vessels being 
blocked by thrombosis. Ergotism causes dry gangrene as a rule ; 
the same may be said of Raynaud's disease. Finally, dry gan- 
grene may result from the moist form when putrefaction is slow 
and evaporation of the fluids occurs. The putrefactive processes 
in the dry type are not marked, and may cease entirely. Dry gan- 
grene is generally circumscribed, and the end-result of a typical 
case is mummification. The color is usually dark, finally black ; 
early it may be yellow or brown ; rarely, the tissues are very pale. 
There is little toxic absorption in these cases. 

Moist gangrene presents numerous varieties. It is rarely pro- 
duced by arterial occlusion, but is the usual result of extensive 
venous occlusion. Internal emboli, as in the pulmonary arteries 
or veins or mesenteric arteries, not infrequently cause gangrene of 
this form. It also occurs in the lungs as a result of ^T^pkational 



RETROGRESSIVE PROCESSES. 



99 



or other pneumonias, abscess, neoplasms, bronchiectasis, and in 
diabetes. It is seen as a result of traumatism and pressure in 
severe contusions (especially with vascular injuries), in intussus- 
ception and strangulation of the bowel; as a result of torsion in 
movable kidneys, spleens, or tumors. It is frequent in the ob- 
structed or strangulated vermiform appendix. Extensive moist 
gangrene of the extremities or other parts is not rare in connec- 
tion with diabetes. The mucous membranes may become gan- 
grenous as a result of various infections. A particular form is 
noma of the mouth and genitalia. It is seen as a rare condition 
in certain skin-diseases ; and is not unusual in severe trophic 
lesions, as decubitus, cystitis, mal perforant, etc. 

In moist gangrene the consistency of the part becomes progres- 
sively softer. There may be local or widespread emphysema. 
The color is usually dark brown, due to disorganized blood-pig- 
ment; the skin commonly becomes black, and is covered with 
blebs. About the area there may be a zone of coagulation-necro- 
sis with vascular thrombosis ; or a zone of inflammatory reaction 
which will produce a line of demarcation. In some cases, espe- 
cially the diabetic, neither of these zones is formed. 

The cells first succumb. The protoplasm and nuclei exhibit 
various evidences of degeneration, the nuclei disappearing and 
the cells becoming converted into granular detritus. Fat and the 
myelin-sheaths of nerve-fibers are reduced to free fat and fatty 
crystals. The muscle-cells lose their striations and become frag- 
mented ; the axis-cylinders of nerves fibrillate. Hemorrhages into 
the area are common, due either to erosion of vessels and expulsion 
of their thrombi by the pressure of the blood-current, or to a genu- 
ine hemorrhagic condition the result of toxemia. Connective tissue 
and elastic fibers resist longer than the cells, but finally become 
liquefied. The affected area contains crystals of pigment, fatty 
acids, cholesterin, leucin, tyrosin, phosphates, and carbonates. 
Ammonia, the fatty acids, indol and skatol, amins, sulphuretted 
hydrogen, carbonic acid, and other gases, usually of pronounced 
odor, are formed. There is more or less toxic absorption from 
these areas. 

But two things can happen to an area of gangrene ; it may 
progress and cause the death of the individual, or may become cir- 
cumscribed. In dry gangrene and in the vascular forms of moist 
gangrene limitation is the rule ; the other moist forms tend to be 
progressive. In the circumscribed form a line of demarcation is 
formed by inflammatory reaction, and the mass is finally cast oif 
as a sphacelus or slough if the area be superficial, or encysted if 
the area be internal. The latter cases may be followed by reab- 
sorption of the contents and calcification of the sac. 



u«rc 



100 



TEXT-BOOK OF PATHOLOGY. 



GENERAL PATHOLOGY OF CELLULAR NECROSIS. 

The cell as an individual element is liable to pathologic processes of 
various kinds that merit brief consideration, apart from definite forms of 
tissue-degeneration and necrosis. 

Etiology. — The causes of cellular degeneration and necrosis are numer- 
ous, including mechanical, thermal, electrical, chemical, and vital (trophic) 
influences of various kinds. It is easy to demonstrate the influence of 
some of these causes in the unicellular organisms such as amebse, and the 
changes thus produced may also be seen under proper conditions in the 
cells of the animal body. 

Pathologic Anatomy. — The cell as a whole may show various forms of 
distortion, or internal change. Increased irritability and mobility of the 
protoplasm cause the projection of pseudopodia, and these may be separated 
from the body of the cell as rounded particles more or less resembling the 
original cell. This is easily demonstrable in red blood-corpuscles sub- 
jected to heat. Sometimes particles of the substances are discharged from 
the cell and vacuolations (expulsion- vacuoles) result. Certain influences, 
like cold, and metallic salts or other poisons, cause a reduced mobility and 
general contraction of the cell. Granular precipitation may at the same 
time occur within the protoplasm. In other cases solution of parts of the 
cellular protoplasm occurs, and vacuoles of varying size are thus produced. 

Similar changes have been discovered in the nuclei of the cells, but 
certain special forms of nuclear change require special mention. 

Nuclear solution or hypochromatosis may occur as a process of gradual 
fading or disappearance. The nucleus becomes more and more pallid, and 
finally is indistinguishable. 

Karyorrhexis is a form of nuclear fragmentation in which the chromatin 
of the nucleus becomes broken up into small particles. 

Hyperchromatosis is a degenerated condition of the nucleus, involving 
the nuclear membrane in particular. The body of the nucleus becomes 
pale and finally quite colorless, while the periphery is much more apparent 
and thickened. With the further destruction of the nucleus and cell the 
pigment-particles arranged around the periphery of the nucleus may become 
scattered through the cell. 

Pyknosis is the name used to designate degeneration of the cell and 
nucleus in which the protoplasmic substance of these structures becomes 
more dense and their size correspondingly decreased. The cells become 
darker and frequently densely granular. When the nucleus is affected this 
contraction may leave a vacant zone about it, so that the nucleus apparently 
lies within a vacuole. 

POST=MORTEM ALTERATIONS. 

Certain changes take place after death which may suggest in their 
appearances ante-mortem disease. It is therefore necessary to recognize 
these in post-mortem examinations. The most striking change is the 
rigidity or rigor mortis, which is due to a coagulation of the muscle-albu- 
min or myosin. This occurs at different intervals, according to the cause 
and nature of death. Sometimes, as in deaths after electrical discharges, 
it occurs almost instantaneously ; more commonly its beginning is delayed for 
some hours. After twenty-four or forty-eight hours the rigidity disappears. 
Occasionally irregular post-mortem contractions of the muscles take place, 
and distortions or even movements are thus produced. 

Circulatory Phenomena. — As is noted elsewhere (see Congestion) the 
blood-vessels, especially the arteries, contract after death, and drive the blood 
into the capillaries and veins. It is then more or less free to sink to 
dependent parts through the influence of gravity, and in consequence the 



RETROGRESSIVE PROCESSES. 



101 



lower parts of the organs and of the body in general are congested. This 
is particularly marked in the lungs, but occurs in practically all organs. 
The blood may remain entirely within the blood-vessels, but not rarely the 
coloring-matter diffuses itself through the tissues and causes pigmented 
areas (livores mortis) that may suggest ante-mortem bruises. < 

The blood in the heart and other vessels tends to coagulate, though in 
some cases this is long delayed and remains imperfect. Usually dark red 
clots are found in the cavities of the heart and in the large vessels. Yel- 
lowish fibrinous clots are less likely to be post-mortem, but more often occur 
in cases in which death has taken a lingering form. 

Post-mortem Degeneration of Tissues. — Some time after death the tis- 
sues may become macerated and putrefactive changes may occur. To a 
large extent these are due to invasion of micro-organisms. It has been 
found that during the terminal stages of disease various forms of infection 
(especially micrococcic) occur. This terminal infection is often the im- 
mediate cause of death, and it is also concerned in the post-mortem change 
in the tissues. Histologically, a striking peculiarity of such post-mortem 
change is the absence of evidences of reaction (cellular infiltration and 
proliferation), such as characterize the response of living tissues to irri- 
tation. 

Post-mortem softening of the mucous membranes may be due to the 
action of the secretions. This is especially marked in the stomach, where 
it is common to observe a macerated condition of the mucosa of the pos- 
terior wall. In this case the gastric juice is the direct cause of the altera- 
tion in the mucous membrane. 



CHAPTER V. 
INFLAMMATION AND REGENERATION. 

INFLAMMATION. 

Definition. — By this name are designated the vascular, exuda- 
tive, degenerative, and regenerative changes which occur in the 
living tissues as a result of irritation by chemical, mechanical, or 
thermal agents. No short definition contains the essence, for in- 
flammation is by no means a simple process. It varies with the 
varying anatomical conditions or the vitality of the tissue involved, 
and with the intensity or nature of the irritant. Galen and his 
followers defined it by giving the cardinal symptoms : heat (color), 
redness (rubor), pain (dolor), and swelling (tumor). To these may 
be added altered function (functio kesa). 

Historical. — The earliest conceptions of inflammation were those of a 
specific entity. Subsequently various theories were offered in explanation 
of the several phenomena or symptoms. First, the blood-vessels were sup- 
posed to be influenced through the nervous system [vascular theories). 
Next, it was taught that the inflammatory irritant excites proliferative 
changes in the tissues (thus giving rise to round cells), and that this stimu- 
lation of the cellular activity invites more blood to the part (hence the 
hyperemia). This was the cellular and attraction theory of Yirchow. 
Others, notably Cohnheim, described the emigration of leukocytes from the 



102 



TEXT-BOOK OF PATHOLOGY. 



blood-vessels, and held this to be the essential feature of inflammation. 
This emigration was first described by Dutrochet (1824), Waller (1842), and 
Strieker ; but Cohnheim was the first to systematize the emigration theory. 
According to Virchow, the first step is a formative stimulation of the cells ; 
according to Cohnheim, degeneration of the vessels leading to emigration ; 
according to AVeigert, at least in many cases, the first step is necrosis of the 
parenchymatous cells. At the present day inflammation is generally re- 
garded as purely reactive in nature, the irritation causing sometimes one 
and sometimes another primary lesion. 

Phenomena in Inflammation. — These may be well studied 
in the mesentery or tongue of a frog. When the mesentery is ex- 
posed and spread under a microscope and a localized area injured, 
the first visible effect is a very temporary contraction of the 
arteries, which may disappear before the examination can be 
made. It is followed by dilatation of the arteries, and then of 
the capillaries and veins. The blood-current is first more rapid 
than normal, then slower, and may finally stop entirely (stasis), 
especially in the capillaries in the center of the inflamed area. 
Notable changes are seen in the circulating corpuscles. It will 
be recalled that under normal conditions the corpuscles circulate 
in the middle of the vascular stream, leaving a clear plasmatic 




Fig. 27.— Inflammation of the mesentery, showing overfilling of the blood-vessels, with 
emigration of leukocytes and diapedesis of red corpuscles (Ziegler). 



zone adjacent to the vessel- wall ; in this zone may be seen occa- 
sional leukocytes travelling somewhat more slowly than the cen- 
tral corpuscular stream. As the current becomes slower the leu- 
kocytes in the plasmatic zone increase in number and stick to the 
vessel-walls in a continuous row. In the capillaries clumps of leu- 
kocytes frequently alternate with masses of red corpuscles, or of red 
and white corpuscles in their customary proportion. Next, it may 
be observed that the leukocytes are passing through the walls of the 
capillaries and veins and spreading in the outside tissues. At the 
same time a certain number of red corpuscles are passed through 



INFLAMMATION AND REGENERATION. 



103 



the capillary walls, and altered plasma escapes and infiltrates the 
tissues. In the connective tissues outside the vessels proliferative 
changes take place, leading to karyokinesis and formation of round 
cells resembling the emigrated leukocytes (Fig. 27). In struct- 
ures in which there are parenchymatous (archiblastic) cells the 
latter undergo various degenerative changes, such as cloudy swell- 
ing, mucous degeneration, fatty degeneration, or even necrosis. 
Less frequently proliferation of the parenchymatous cells takes 
place. Every case of inflammation does not present all of these 
phenomena, nor is the subsequent fate of the exudate and altered 
cells always the same. 

The phenomena must now be separately considered. 

1. Changes in the Vessels. — The first effect of irritation maybe 
momentary contraction of the arteries ; but this is rarely observed. 
Usually the arteries dilate at once, and dilatation of the capillaries 
and veins promptly follows. The cause of this dilatation was for- 
merly looked for in the nervous system, but it is more probably 
to be found in some degeneration of the vessel-walls. The micro- 
scope does not reveal this, but some of the phenomena connected 
with exudation and the circulation of the blood show that the 
cause must be in the vessel-walls. There are certain visible 
changes in the vessels, such as swelling of the endothelial cells 
and increase of the intercellular spaces, and some undoubted 
though invisible changes, such as increased adhesiveness of the 
endothelial cells. 

2. Exudation. — The blood-current is at first more rapid, then 
slower, than normal. The former is due to dilatation of the 
arteries ; the latter doubtless to some change in the walls of the 
blood-vessel increasing the friction. Mere dilatation of the vessels 
could not affect the current in this way. As the current grows 
slower the leukocytes in the plasmatic zone of the blood-stream 
increase in number and cling to the wall of the vessel. This is 
purely a mechanical result of the slower rate of the blood-current. 
Finally, the leukocytes pass through the vessel-walls between the 
endothelial cells and collect on the outside of the blood-vessel, 
whence they more slowly migrate through the tissues (Fig. 27). 
This emigration of leukocytes occurs to a moderate degree normally, 
but is abnormal in degree in inflammation. Cohnheim ascribed it 
to disease of the vessels — increased permeability — the leukocytes 
being purely passive. Later observation indicates that the chief 
role in this excessive emigration must be assigned to the stimu- 
lated ameboid movements of the leukocytes. Degeneration of 
the vessel-walls, especially swelling and softening of the cement- 
substance between the endothelial cells, and the pressure of the 
blood, aid ; but only to a minor extent. The cause of this active 
ameboid motion and tendency to emigration has recently been 
found to be an attractive force peculiar to the causes of inflam- 



104 



TEXT-BOOK OF PATHOLOGY. 




mation. Stahl, and later Pfeffer, found that certain substances 
exert an attractive or repellent force upon low forms of vegetable 
and animal life, upon spores of plants, and upon bacteria. To 
this force the name chemotaxis has been given, and the terms posi- 
tive and negative chemotaxis are 
used to designate the attraction 
and the repulsion respectively. 
Positive chemotaxis is an un- 
doubted and satisfactorily de- 
monstrated force ; but negative 
or repulsive chemotaxis has not 
been proved. The irritant sub- 
stances which cause inflamma- 
tion are probably positively 
chemotactic in action ; and in 
cases in which mechanical in- 
jury causes inflammation, such 
substances first result from 
mechanical destruction of cells 
and then occasion the subse- 
quent phenomena of inflamma- 
tion. In other inflammations 
the irritant causing the disorder 
may itself contain the posi- 
tively chemotactic substance 
(see under Suppurative Inflam- 
mation). The microscopic ap- 
pearance of the tissues after 
emigration of the leukocytes 
is characteristic. The capil- 
laries are dilated and obscured 
by a mantel of exuded white 
corpuscles, and the tissue 
around is infiltrated with mi- 
gratory leukocytes. This ap- 
pearance is called round-cell 
infiltration or inflammatory in- 
filtration (Fig. 28). The round 
cells are mostly polymorphous 
leukocytes, a few are lymphocytes, and some are new-formed con- 
nective-tissue cells, as will be subsequently described. 

Plasma- cells. — The cell described under this term by Unna is a small cell 
whose protoplasm stains a violet-blue with methylene-blue. There are no 
distinct granules, though sometimes the protoplasm is slightly granular. 
The nucleus is usually excentrically placed and surrounded by dark masses 
of chromatin. The cell varies in size from that of the small lymphocyte to 
that of a large mononuclear leukocyte. Karyokinesis has been observed in 
a few cases. The plasma-cell is probably an altered lymphocyte which has 




Fig. 28.— Acute appendicitis, with exten- 
sive round-cell infiltration of all of the coats 
of the appendix. 



INFLAMMATION AND REGENERATION 



105 



escaped from the blood-vessels. Some hold that it is a form of connective- 
tissue cell and that it is concerned in regeneration of connective tissue. 
This is unproved. The plasma-cell is found in inflammatory exudates of 
all sorts and in the lesions of the infectious diseases — tuberculosis, leprosy, 
syphilis, etc. 

The plasma-cell of Waldeyer is different from that above described. It 
is identical with the mast-cell of Ehrlich. This is a cell containing large 
basophilic granules. (See Diseases of the Blood.) It occurs in inflamma- 
tory processes of a chronic character and in various tumors and degenera- 
tive lesions. . Its significance and nature are uncertain. 

Coincidently with leukocytic emigration there is exudation of 
more or less altered blood-plasma. This is richer in albumin and 
more coagulable than dropsical fluid, which is a further indication 
that the blood-vessels are more permeable in inflammation than in 
health or mere congestion. It is probable, moreover, that the 
capillary walls act in a secretory manner, as do the walls of the 
lymphatic channels. This would in some measure explain the 
difference between inflammatory transudates and dropsical liquids. 

Finally, a certain number of red corpuscles escape from the 
capillaries by diapedesis. This is a purely passive process so far 
as the red corpuscles are concerned, being due to pressure of the 
blood. It is particularly marked when stasis has occurred. Ac- 
cidental hemorrhage by rhexis may add to the blood in an exudate, 
but this is not a truly exudative process. 

3. Degenerative Changes in the Tissues. — The action of the irri- 
tants which excite inflammation sooner or later affects the tissues 
and causes degeneration or death. The first effect may fall upon 
the blood-vessel walls or upon the tissues. Weigert, Neumann, 
and others hold that the " primary effect" in inflammation is 
generally or always this tissue-degeneration, which excites second- 
ary proliferation. This is certainly the case at times ; and the 
discovery that tissue-degeneration leads to the formation of sub- 
stances positively chemotactic in action would indicate the manner 
in which inflammation is brought about in these cases. The degen- 
erative changes may be merely physiologic (some form of altered 
functional activity), or there may be structural alterations, such as 
cloudy swelling, liquefaction, fatty change, coagulation- or other 
forms of necrosis. The nature of the degeneration depends largely 
upon the severity of the irritation. Very powerful irritants cause 
necrosis at once, and not inflammation. It is the irritants which 
disorder, but do not entirely destroy, cells that are especially apt to 
excite inflammation. The condition of general and local vitality 
is of great importance in determining the extent of the degenera- 
tive change in the tissues. Thus, in states of reduced general 
vitality catarrhal inflammations with extensive epithelial degenera- 
tion may be very persistent, and may subside promptly when the 
general health is improved. 

4. Proliferative Changes. — Sooner or later in an inflamed area 
there are evidences of cellular proliferation, which occasions the 



106 



TEXT-BOOK OF PATHOLOGY. 



appearance in the tissue of round cells closely resembling the out- 
wandered leukocytes. They differ, however, in being somewhat 
larger, in having a larger and paler nucleus, which is rounded or 
oval, and in their frequently exhibiting evidences of karyokinesis. 
The round-cell infiltration of the chronic inflammations, in which 
proliferation of the connective tissue is conspicuous, differs from 
that of acute inflammations in the predominance of leukocytes of 
the lymphocytic form. These cells are derived from pre-existing 
connective-tissue cells. Recently a fanciful theory teaches that they 
are in part redevelopmentsof cellular remnants which had almost or 
quite lost their cellular character, such as fibrillar protoplasmic pro- 
longations of connective tissue. These are the "slumbering cells" 
of Grawitz. Virchow held the proliferative changes to be the essen- 
tial feature in inflammation, and believed that all round cells have 
this origin; Cohnheim denied the occurrence of proliferation, and 
ascribed to emigration the essential role. Later, it was held that 
the proliferative changes are not in reality a part of inflammation, 
but rather regenerative and for the purpose of repairing the tissue- 
injuries after inflammation (Fig. 29). At the present time we 



' St i> ^ f - * - ■ 



Fig. 29.— New blood-vessels and fibroblastic cells in a beginning adhesion of the peri- 
cardial layers. 

must regard as factors in inflammation both emigration and pro- 
liferation, whether the latter in any individual case is due to direct 
stimulation of the cells, or is secondary to destructive changes, or 
is merely the result of increase of nutrition from the inflammatory 
congestion. It is conjectured by some that under chemotactic 
influences the cell-contents of fixed cells are incited to movements 
terminating in karyokinesis, just as the whole cell is influenced in 
the case of movable cells. Proliferative changes also occur in the 
parenchymatous cells, but in that case they are more strictly regen- 
erative in nature. 



INFLAMMATION AND REGENERATION. 



107 



Etiology. — Irritation by mechanical, chemical, thermal, or in- 
fectious agents causes inflammation when it is severe enough to dis- 
turb the vitality of the tissue and not sufficient to cause extensive 
necrosis at once. When the irritant is brought to bear upon the 
tissues directly, there is probably, first, cell-degeneration, fol- 
lowed by vascular disturbances and emigration. When the irri- 
tant acts through the blood, vascular disorders probably, as a rule, 
precede the tissue-changes. Micro-organisms may act by first de- 
stroying the cells, or may by their own death liberate from their 
substance some poison (protein) which is chemotactic. Disturb- 
ances of circulation, innervation, or metabolism may so alter cel- 
lular processes as to occasion the production of irritating and 
chemotactic products. * 

Special Forms of Inflammation. — Various classifications 
may be used in describing forms or types of inflammation. The 
most natural is that which follows the anatomical changes. Thus 
we may distinguish (1) exudative inflammation, or the form in 
which the fluid and cellular exudation from the blood-vessels is 
the predominating element in the pathologic process ; (2) paren- 
chymatous or degenerative inflammation, or the form in which 
destruction of the parenchyma cells is the leading feature ; and 
(3) productive inflammation, in which proliferation is the striking 
characteristic. The nature of the cause, as well as the resistance 
of the organism or of the affected part, determines the particular 
form in a given case. 

A number of sub-varieties may be described, but it must always 
be remembered that the three processes exudation, degeneration, 
and proliferation are present in greater or less degree in all forms. 

Types of Inflammation. — 1. Edematous or serous inflamma- 
tion is characterized by a copious exudation of fluid with com- 
paratively little cellular matter, as in edema of the larynx, serous 
effusions in the serous sacs, etc. The local forms of edematous 
or serous inflammation are usually expressions of intensely irritant 
causes ; the serous inflammations of serous cavities, however, are 
not necessarily of this severe grade. Indeed, in many cases serous 
inflammation may be a mild subacute or chronic process, which may 
subside gradually, leaving the serous membranes slightly thick- 
ened or adherent. The fluid in inflammatory exudations differs 
from dropsical fluid in containing more albumin and fibrin- 
factors. 

2. Fibrinous Inflammation. — The plasmatic exudate may clot 
at once and form a fibrinous membrane on free surfaces or a net- 
work within the tissues ; this is termed fibrinous inflammation. 

In purely fibrinous inflammations of serous surfaces there is a 
whitish or yellowish-white deposit of variable thickness which is 
more or less adherent to the underlying surface. When removed, 
there is seen beneath it a variably pronounced injection of the 



108 



TEXT-BOOK OF PATHOLOGY. 



blood-vessels and roughness and rawness of the surface. This is 
due to beginning granulations (see Repair of Wounds). Micro- 
scopically the fibrinous deposit consists of an irregularly arranged 
mass of fibrillar, granular, or homogeneous fibrin, with leukocytes 
and endothelial cells (more or less degenerated) enclosed in the 
deposit. Fibrinous inflammation is often associated with serous 
exudation, and the term sero-jibrinous is applied. In other cases 
(especially in peritoneal inflammations) the exudate is likely to 
become purulent — -fibrino-purulent inflammation. 

Inflammations of the serous membranes are nearly always 
more or less fibrinous, and croupous pneumonia is a typical 
example. 

It is doubtful if fibrinous inflammation can ever occur independently of 
destruction of the fixed cells. In other words, it is doubtful if the fibrinous 
exudate is ever purely an exudate. Some experimenters have described 
fibrinous inflammations of serous surfaces with an unbroken lining of 
endothelial cells under the fibrinous deposit, and have concluded that the 
fibrin is wholly exudative. Others regard the large cells as cells of lymph- 
spaces, and not the original surface cells ; and consequently conclude that 
cellular destruction plays a part in the fibrin-formation. 

3. Diphtheritic inflammation differs from the last in having 
associated with the coagulation of the exudate coagulation-necrosis 
of the cells of the part inflamed. Diphtheritic inflammation 
occurs especially in the pharynx and larynx, where it occasions 
pseuclomembranes (Fig. 30). This is most frequently due to the 




Fig. 30. — Pseudomembranous inflammation of the uvula: a, masses of micrococci; 6, 
necrotic cells ; c, round-cell infiltration ; d, fibrin-network (Ziegler). 

specific cause of the disease called diphtheria ; but diphtheritic in- 
flammation may result from a variety of severe irritations, such as 
bacteria, superheated steam, and chemical irritants. The diphthe- 
ritic membrane consists of a network of fibrin or of homogeneous or 



INFLAMMATION AND REGENERATION 



109 



granular fibrin-masses enclosing degenerated epithelial cells and 
emigrated leukocytes. Sometimes it is quite superficial, involving 
only the surface-layer of epithelium ; at other times the whole 
depth of the mucous membrane is implicated. The former are 
sometimes called croupous and the latter diphtheritic false mem- 
branes. These terms, however, are ill-defined and objectionable. 

4. Suppurative inflammation is characterized by unusual abun- 
dance of emigrated leukocytes and by the tendency to lique- 
faction. Bacteria are most frequently the cause ; but it has 
been shown experimentally that croton oil, calomel, turpentine, 
and other substances are capable of producing suppuration. Of 
the bacteria, the commonest are the so-called pyogenic staphylo- 
cocci and streptococci ; but numerous forms, not essentially pyo- 
genic, may occasionally prove so. Such are the bacillus of 
typhoid fever, the gonococcus, the Bacillus coli, and others. 
Recent studies ascribe to chemotaxis the important role in the 
action of bacteria in inflammation and suppuration. Either the 
products of the bacteria or substances derived from their own 
protoplasm (bacterioprotein — Buchner) exercise a powerful chem- 
otactic influence, and thus occasion the massing of emigrated 
leukocytes (Fig. 31). The same or similar substances further 




Fig. 31.— Embolic abscess in the myocardium, showing accumulation of large numbers of 
leukocytes (Karg and Schmorl). 

prevent fibrin-formation or cause a solution of fibrin already 
formed, and thus the exudate liquefies and forms pus. This con- 
sists of a liquid part, the liquor puris, a modified blood-plasma, 
which differs from ordinary plasma in being less coagulable and 
containing notable quantities of albumose (peptone), and a corpus- 
cular part, consisting chiefly of multi nuclear leukocytes more or 
less degenerated. Some proliferated connective-tissue cells or 
wandering cells may be added from the neighboring tissue, but 
these are very few in number. 



110 



TEXT-BOOK OF PATHOLOGY. 



The entrance of bacteria of suppuration into the body may take 
place directly through wounds, or somewhat indirectly through 
small abrasions in the various mucous membranes. Some local 
injury may serve to determine the suppurative inflammation at a 
given place. 

Abscess. — When suppuration occurs in the substance of a tissue 
or organ, the lesion is called an abscess. This consists of a collec- 
tion of pus, which usually presents a creamy yellow color, but 
may be variously altered in odor or color by subsequent changes. 
Around the abscess the tissues present the proliferative changes 
described as part of inflammation. There are numerous round 
cells, differing from emigrated leukocytes and showing karyo- 
kinetic figures in the nuclei, and there are new blood-vessels and 
beginning organization (see Regeneration). This restraining wall 
of granulation-tissue was formerly regarded as a pus-producing 
membrane, and therefore called the pyogenic membrane. Ab- 
scesses, especially such as are due to bacteria, tend to soften the 
surrounding tissues in the direction of least resistance, and thus 
to break on the surface, discharging their contents by sinuous 
tracts or sinuses. Sometimes the pus of an abscess becomes in- 
spissated by absorption of the liquid part, and the residue under- 
goes various degenerative changes, such as mucous, fatty, or 
calcareous. At the same time the surrounding membrane ad- 
vances to complete organization, and thus encapsulates the 
abscess. 

Ulcer. — Suppurative inflammation with erosion of areas of the 
skin or mucous surfaces occasions ulcers. These have the same 
histologic construction as the wall of an abscess, the base of the 
ulcer being the same as the pyogenic membrane. In it may be 
seen small red points or granulations, which consist of loops of 
capillary blood-vessels surrounded by round cells. (The his- 
tology of granulation-tissue is more minutely described under 
Regeneration.) 

The appearance and pathologic course of ulcers vary widely. Some- 
times rapid destruction of the tissues causes large and spreading ulcers, 
called phagedenic. Others extend in one direction while healing in other 
parts, and are called serpiginous. The granulations may be too rapid in 
growth, forming red fungous masses (proud flesh) which fill up the ulcer. 
In other cases the ulcer remains dry and indolent, showing little tendency to 
heal. 

Some ulcers are not primarily of inflammatory origin. For example, the 
round or peptic ulcer of the stomach is formed by digestion, through the 
action of the gastric juice, of a part of the stomach which has become 
lowered in vitality or possibly necrotic. Similarly, the beginning change in 
the perforating ulcer of the foot in tabes and in decubitus (bed-sores and 
other forms of pressure ulceration) is not inflammatory, but rather necrotic. 

Suppurative inflammations of serous membranes lining closed 
sacs cause collections of pus in the cavities. The pus usually 



INFLAMMATION AND REGENERATION 



111 



contains more or less fibrin, and there is a fibrino-pnrulent exu- 
date on the serous surface. 

Suppurative inflammation of the skin and subcutaneous tissues 
may be localized or diffuse. Of the localized type there are 
various pustules, furuncles or boils, and carbuncles. 

A furuncle is a suppurative and necrotic inflammation be- 
ginning in one of the sweat-glands, sebaceous-glands, or hair- 
follicles. A carbuncle is a more extensive but similar process 
beginning in several of the glands or hair-follicles simultaneously, 
and causing considerable necrosis or gangrene of the skin and 
subcutaneous tissue. 

5. Catarrhal Inflammation. — This term is used to designate in- 
flammations of mucous membranes. The character of the inflam- 
mation depends to a large extent upon the individuality of the 
mucous membrane affected, differing greatly in the nose, throat, 
stomach, bowel, etc. There is always considerable congestion of 
the mucosa, and generally a great deal of serous exudation, which 
is discharged from the surface as a rule, but is to some extent 
retained in the tissue, causing edematous swelling. This is 
especially marked when the submucosa is considerably implicated. 
The epithelial cells of the surface suffer degeneration (mucous or 
fatty) and necrosis, and are discharged with the serous exudate ; 
they may be recognized as goblet-cells (mucous) or as granular 
cells (fatty) or as fragmented necrotic structures. Coincidently 
with the serous exudation, and in greater measure after the latter 
has become less marked, leukocytes escape from the blood-vessels 
or emigrate from their resting-places in the submucosa and make 
their way to the surface between the epithelial cells (Fig. 32). 
"When in great abundance (as in some nasal catarrhs) the process 
may be a purulent or suppurative one ; more frequently there is 
sufficient mucus to require the term muco-purulent. Superficial ero- 
sions of the epithelium and hemorrhages are frequently met with. 

"When catarrhal inflammations are chronic, there is always con- 
siderable productive inflammation, with consequent thickening, and 
later, when the new fibrous tissue contracts, thinning of the 
mucosa. When the contractions of the fibrous tissue are irregu- 
lar, the mucosa between the fibrous areas may be elevated, 
especially if there is at the same time proliferation of the surface 
epithelium and the glandular elements in the mucosa. In such 
cases a granular surface or polypoid elevations result. These are 
common in the stomach and the bowels. 

6. Parenchymatous or Degenerative Inflammation. — This term 
may be applied to certain inflammations, such as forms of 
nephritis, in which degeneration (cloudy, fatty, etc.) of the 
parenchyma-cells is more conspicuous than the exudative pro- 
cesses. The term diffuse inflammation is more appropriate. 

7. Productive Inflammation ; Chronic Inflammation. — In this 



112 



TEXT-BOOK OF PATHOLOGY. 



form the proliferative changes predominate over exudation and 
degeneration. This may be due to the extent of the primary 
tissue-injury or to the nature of the cause. Whether the regen- 
erative processes are always reactive and consequent upon primary 




Fig. 32.— Acute bronchial catarrh, showing the escape of leukocytes from the submucous 
tissue between the epithelial lining cells (Thoma). 

destruction, or may be stimulated directly by the irritant, is un- 
settled. This form of inflammation is often called interstitial when 
occurring in the substance of organs. 

Repair of Wounds. — Productive inflammation is well illus- 
trated in the healing of wounds. If the lips of a clean, incised 
wound are drawn together at once and kept closely apposed, rapid 
healing occurs, which is called healing by immediate union. In 
these cases a microscopic examination shows slight exudation from 
the surfaces of the wound and proliferated connective-tissue cells. 
The epithelial continuity is restored by proliferation of the old 
epithelial cells. Should apposition be less immediate or less accu- 
rate, the amount of exudation is greater. If the wounded surfaces 
are examined twenty-four hours after the injury, they are found 
red and swollen and soon they become glazed in appearance. The 
microscopic features here are the same as in the case of healing by 
immediate union, excepting the amount of exudation is greater. 



INFLAMMATION AND REGENERATION. 



113 



Healing proceeds in the same way but more slowly, and is called 
healing by first intention. In neither case is there great congestion. 
If the wound be irritated by foreign bodies or kept exposed, there 
will be seen on the surfaces, after two or three days, small red 
elevations, known as granulations, which 
consist of loops of new-formed capillaries 
covered by emigrated and new-formed 
round cells, and sometimes (after longer 
intervals of time) giant-cells (Fig. 33). 
The surface may be covered with pus. 
The proliferated round cells gradually 
elongate and form new fibrous tissue (see 
Regeneration), which afterward contracts, 
forming cicatrices or scars. The epithelial 
continuity is re-established by multipli- 
cation of the old epithelial cells at the 
edges of the wound. This form of heal- 
ing is called healing by second intention 
or healing by granulations. 

The formation of adhesions follow- 
ing inflammation of the serous surfaces occurs in much the same 




Fig. 33.— Loops of blood- 
vessels in granulation-tissue 
(Thiersch). 




Fig. 34. 



-Adhesive pericarditis, showing fibrin-deposit, with new blood-vessels extending 
upward into it (Perls). 



way as wounds heal. The primary exudation is largely fibrinous 
and causes agglutination of neighboring surfaces. Subsequently 
the proliferated connective-tissue cells penetrate this fibrinous ex- 
udate, as do newly-formed blood-vessels (Fig. 34). Thus a union 



114 



TEXT-BOOK OF PATHOLOGY. 



of vascular channels is effected between the adjacent inflamed 
surfaces and organization follows. 

Precisely similar changes occur in the tissues surrounding a foreign body, 
as a piece of sponge, or around a portion of dead tissue. In these cases the 
exudative and proliferated cells tend to penetrate into the foreign mass, as 
occurs also in the organization of thrombi. There is also in these cases a 
greater tendency to the formation of giant-cells (by division of nuclei with- 
out division of the cell-body) than in ordinary granulations. If the foreign 
mass can be softened and absorbed, this gradually occurs, and later merely 
a scar will remain ; if it cannot be absorbed, connective tissue encloses or 
encapsulates it. 

General Fibrosis. — A tendency to widespread productive in- 
flammation is noted in certain individuals. This affects the blood- 
vessels especially (general arteriocapillary fibrosis, general angio- 
sclerosis), and also the liver (cirrhosis of the liver), the kidneys 
(interstitial nephritis), and other organs (Fig. 35). The cause of 
these changes is supposed to be some general intoxication — 
alcoholic, gouty, syphilitic, or the like. 




Fig. 35.— Chronic interstitial nephritis : ?reat increase of connective tissue around the 
glomeruli, renal tubules, and blood-vessels ; from a case of arteriocapillary fibrosis. 

Productive inflammation may affect other tissues than the fibrous 
connective tissues. Reference has already been made to epi- 
thelial proliferation in the healing of wounds. Similar epithelial 
processes of greater activity or duration may lead to warty growths 
of the skin or polypoid outgrowths on the mucous membranes. In 
pharyngeal catarrhs considerable proliferation of the adenoid tis- 
sues is not unusual. So also thickening of cartilages, bones, or the 
periosteum is not an unusual result of inflammation of these 
structures. 



INFLAMMATION AND REGENERATION 



115 



8. Hemorrhagic Inflammation. — More or less diapedesis of red 
corpuscles generally occurs in inflammation ; but sometimes the 
irritating cause falls with such peculiar force on the blood-vessels, 
or the general condition of the patient (cancer, tuberculosis, hemo- 
philia, scurvy) is so unsatisfactory that the exudate is unusually 
rich in red corpuscles. These are always serious inflammations, 
and are to be distinguished from ordinary inflammations in which 
accidental hemorrhage occurs. 

9. Necrotic or gangrenous inflammations likewise depend for 
their occurrence upon the severity of the irritation or the state of 
the general system. 

Pathologic Physiology and Pathogenesis. — Inflamma- 
tion represents increased and altered activity of tissues as a result 
of irritation ; its primary object is the removal of the irritant. 
In this process no new forces or activities are involved : the 
phenomena are all observed in normal tissues, though to a less 
degree and in more orderly behavior. The liquid and cellular 
exudation has its prototype in the formation of lymph and in the 
normal wandering cells of the tissues ; the increased vascularity is 
the result of increased demand, and is abnormal in degree only ; 
the cellular destruction is an accentuation of the ordinary death 
of cells resulting from wear and tear, though the form of the cell- 
destruction is more violent and probably different ; the post-in- 
flammatory regeneration is effected by karyokinetic multiplication 
of cells, as in normal tissues. 

In the removal of the irritant, phagocytosis (q. v.) is im- 
portant ; it is accomplished by the leukocytes, and to a less extent 
by endothelial cells and wandering connective-tissue cells. 

The functional activity of a part the seat of inflammation is 
often increased, though somewhat altered. An inflamed gland 
may produce an excessive but abnormal secretion. In other cases 
functional activity is lessened ; chronic inflammations almost cer- 
tainly lessen functional action. 

Resolution after Inflammation. — In cases of trivial 
exudation the emigrated leukocytes may re-enter the blood-cur- 
rent or may escape through the lymphatics. The liquid exudate 
is similarly disposed of ; while the proliferated connective-tissue 
cells (if there be any proliferation) remain in loco or become 
wandering cells. When the exudate is more abundant the liquid 
elements may be removed in the same way, but the cells first 
undergo degenerative softening and are reduced to the form of an 
emulsion, which is gradually absorbed. The degenerated paren- 
chyma in inflammation may recover if the degeneration is not 
severe, or may be softened and removed. Phagocytic cells often 
play a prominent part in the removal of broken-down cellular 
remains, pigment-masses, and the like. 

The reparative changes in inflammation may be so slight as to 



116 



TEXT-BOOK OF PATHOLOGY. 



lead to no discoverable lesion after the process is completed ; 
but when large damage has been done there is apt to be a perma- 
nent scar or some other productive lesion. 

REGENERATION. 

Definition. — The term regeneration is applied to the forma- 
tion of new cells or tissues to take the place of those destroyed. 
Regeneration may be physiologic or pathologic. The former is 
that which occurs in the normal life of the organism and by which 
the cellular wear and tear is counterbalanced. Pathologic regen- 
eration is the more massive and often atypical reconstruction that 
follows disease or injuries. 

etiology. — The cause or mechanism by which normal regen- 
eration is brought about is more or less obscure. The cells have 
an inherent tendency to multiply, and this goes on to a certain 
point at which the normal development is complete. This limit is 
probably maintained by some restraining influence, but the nature 
of this is unknown. In the skin and mucous membranes, where 
physiologic regeneration is most active, new cells are constantly 
produced and the older cast off. In what manner the balance is 
so maintained that production and destruction keep their equal 
pace is as yet matter only for speculation. The idea of action and 
reaction occurs naturally to the mind, and it seems probable that 
the reproductive processes are dependent in some way upon the 
loss of substance. In some cases the normal restraining influence 
seems to be deficient and giant-growth results. In all forms of 
normal or physiologic regeneration the reconstructed cells are 
exactly like the pre-existing cells, and the status of the tissue is 
unaffected. In highly-specialized cells, such as those of the 
nervous system, regeneration seems to be intracellular — that is, 
the cells are constantly rejuvenated by supplies of nutriment 
rather than reproduced in toto. 

In pathologic regeneration there seems to be abnormal stimu- 
lation of the reproduction of cells as well as a reduced restraint. 
It is not improbable that various toxic substances have the power 
of stimulating the formative process, though this has not been 
actually demonstrated. In all cases in which regeneration follows 
mechanical, thermal, or toxic causes there is, first, destruction of 
cells, and following this regeneration. In such cases the relief 
from the accustomed pressure may serve as a withdrawal of re- 
straint, but at the same time there is doubtless augmented form- 
ative energy. The latter may result from the same agency as 
that which caused the primary cell-destruction, or it may be due 
to the influence of formative irritants derived from the dying and 
dead cells. The demonstration that micro-organisms are able to 
produce substances having a strong attractive or repellant influence 



INFLAMMATION AND REGENERATION 



117 



upon leukocytes gives some warrant to the belief tnat similar sub- 
stances are at work in the regenerative changes that accompany 
bacterial diseases. In the case of tissue-destruction due to other 
causes similar products possibly play a part. 

Pathologic Anatomy. — In the normal regeneration of cells 
the process is one of gradual cell-multiplication without marked 
changes of any sort. Pathologic regeneration may be equally 
simple, but more often there are complicated changes in the pre- 
existing tissues and new formation of blood-vessels preceding or 
accompanying the regeneration. The vascular regeneration is a 
necessary preliminary, having the purpose of supplying abundant 
nutriment to the tissues undergoing proliferation. 

Cell-multiplication occurs in two ways, the direct and the in- 
direct. The former method is one of simple cleavage, by which 
the cell is divided into two or more parts. This mode of division 
is unusual. The common method is called indirect segmentation, 
karyokinesis, or karyomitosis. In this method complicated changes 
begin in the nucleus and finally lead to division of the cell into 
two or rarely into several parts. It is unnecessary to refer to the 
histologic stages in detail, but in a general way we may describe 
the process as follows : (1) the nucleus of the cell enlarges and the 
chromation-fibers become thicker and less closely woven than 
normally ; (2) U-shaped loops of chromatin-fibers arrange them- 
selves around a central clear space or polar field to form a mother- 
wreath ; (3) these loops then undergo longitudinal cleavage and 
the separated parts move one to one pole and the other to the 
opposite pole of the cell, forming daughter-stars, which eventually 
become coarse and then fine skeins of new nuclei ; (4) the proto- 
plasm of the cell finally divides and the process becomes complete. 

Abnormal Cell-division. — There are certain disorders of cell-multiplica- 
tion that may be here described. Karyokinesis, instead of being a regular 
process of division of the nucleus into two daughter-uuclei, may proceed 
irregularly. Sometimes the process is asymmetric — i. e. does not lead to 
equal division ; in other cases it is multipolar, several instead of two 
daughter-nuclei resulting. Other less definite irregularities are sometimes 
observed, and some have held that cell-division may occur by a process of 
mixed karyokinesis and amitosis. It is important to recognize that some 
of the forms of nuclear degeneration (karyorrhexis ; hyperchromatosis) 
may be mistaken for normal or abnormal karyokinesis. Pathologic karyo- 
kinesis is most frequently seen in malignant tumors. 

Pathologic Regeneration. — In the reconstruction of areas of 
destruction of surface-epithelium (mucous membranes, skin) the 
process of cell-multiplication, as above described, occurs in the 
epithelial cells under and around the area of destruction, and 
eventually the surface is fully restored. The same form of regen- 
eration may occur in other surface-cells, as those of serous mem- 
branes, and also in the substance of organs or solid tissues when 
the cellular damage is slight. In cases of more extensive destruc- 



118 



TEXT-BOOK OF PATHOLOGY. 



tion the connective tissues play an active part and the restoration 
is atypical, the new-formed tissue containing a greater amount of 
connective tissue than the pre-existing tissue. In the case of 
highly specialized tissues, such as the gray matter of the brain or 
cord, the regeneration is confined to the supporting tissues. In 
massive regeneration or regeneration of specialized tissues, then, 
the principal changes are those affecting the connective tissues. 

Regeneration of Fibrous Connective Tissues. — It is difficult to 
draw a line between the process of inflammation and regeneration. 

In the latter process there is al- 
,0--\ ways some congestion and cellular 

infiltration (emigration of leuko- 
cytes) ; later, multiplication of the 
fixed connective-tissue cells and 
new formation of blood-vessels 
occur. 





Fig. 36. — Formation of new blood- 
vessels, as seen in the tail of a tadpole 
(Arnold). 



Fig. 37.— Fibroblasts forming fibrous tissue 
(Ziegler). 



The multiplication of connective-tissue cells may be more or less 
abundant. The old connective-tissue cells swell and the nuclei 
divide by karyokinesis, new cells of rounded outline and with rather 
pale nuclei resulting. At the same time the cells of the capillary 
blood-vessels become swollen and here and there budding pro- 
cesses are sent outward (Fig. 36). These may unite with similar 
processes from an adjacent or the same capillary and then undergo 
central vacuolization, which proceeds along the loop, converting it 
into a channel with here and there new-formed nuclei within the 
protoplasmic wall. The latter finally becomes differentiated into 
definite endothelial plates and the new capillary is completed. 
Around these capillary loops lie the emigrated leukocytes, and 
especially the new-formed connective-tissue cells. The latter are 
the formative cells of the regenerating tissue. In the case of 
fibrillar connective tissues they are called fibroblasts (Fig. 37). 
The process is practically the same in the different varieties of 
connective tissue, the differentiation occurring secondarily. The 
formative cells become larger and more or less elongated, and the 



INFLAMMATION AND REGENERATION. 



119 



formation of intercellular substance then follows. In the case of 
fibrillar connective tissue the cells elongate considerably, and by 
segmentation of their extremities in part contribute to the forma- 
tion of the intercellular fibrils. The rest of the fibrils are formed 
by cleavage of the homogeneous intercellular substance in which 
the cells are at first embedded. This intercellular substance, in 
part at least, is doubtless a product of cellular activity. 

When the processes of regeneration have reached this stage 
the new-formed tissue consists of an abundance of round and 
elongated cells, with a small amount of fibrillar intercellular 
substance. Subsequently the latter increases in amount and by 
contraction further adds to its density. During this late stage the 
number of cells becomes less considerable, and eventually there 
may be only here and there a cell embedded in dense bands of 
fibrils. Nearly always, however, there is greater cellular richness 
in new-formed connective tissues than in the normal tissues of the 
same kind. 

Regeneration of other Connective Tissues. — The reconstruction 
of cartilage and bone may occur by primary formation of ordi- 
nary connective tissue and subsequent transformation. This 
is especially the case when the regeneration springs from the 
periosteum or from membranous connective tissues. In other 
cases, however, the regenerative processes produce cartilage and 
bone directly. In the regeneration of fatty tissue there is first 
formed an ordinary connective tissue, and subsequently the fatty 
deposit occurs within the cells. 

Regeneration of Parenchymatous Tissue. — When connective- 
tissue regeneration follows lesions of the parenchymatous organs 
the cellular elements of the latter are reproduced in some measure 
at the same time that connective-tissue hyperplasia is taking place. 
The degree of restoration of the normal structure on the one hand 
or of formation of connective tissue on the other hand depends 
upon the intensity of the original cause of destruction and the 
extent of the injury. In glandular organs reproduction of acini 
may occur to a considerable extent, but these are usually atypical 
in character. In some cases this atypical glandular formation 
may become pronounced, and an adenomatous structure may 
result. (For further details regarding this, see Adenoma.) 

Regeneration may occur in practically all of the tissues of 
the body, though in a varying degree. It has not been shown, 
however, that the large nerve-cells are capable of proliferation, 
though the occurrence of such cells in certain tumors suggests 
the possibility. 



120 



TEXT-BOOK OF PATHOLOGY. 



METAPLASIA. 

Metaplasia is the term applied to the transformation of one 
form of tissue into another without the intervention of a stage of 
regeneration by cellular multiplication. In many instances the 
change consists of a transformation of the intercellular substance, 
as, for example, when ordinary connective tissue is converted into 
myxomatous tissue, or fibrillar connective tissues are altered to car- 
tilaginous or even bony tissue. The cells themselves suffer second- 
ary changes. In other cases of metaplasia the cells may be 
primarily altered, as when ordinary connective tissue is changed 
to fatty tissue. 



CHAPTER VI. 

PROGRESSIVE TISSUE=CHANGES. 

This term may be used to designate pathologic conditions in 
which there is a decided tendency to formation of new tissue. 

HYPERTROPHY. 

Definition. — The term hypertrophy is applied to a pathologic 
condition in which a certain part increases beyond the normal 
size, without marked alterations from the normal structure. The 
term hypertrophy is frequently used loosely to designate enlarge- 
ments of various kinds in which but one tissue of an organ is 
increased, or in which there is deposit of abnormal exudate. Such 
instances are not, strictly speaking, cases of hypertrophy. 

Etiology. — The causes of hypertrophy are quite numerous. 
In some cases there is a distinct increase of functional demand 
brought about in some way or other, as in the hypertrophy of the 
muscles of athletes ; in the hypertrophy of a kidney after disease 
or removal of its fellow ; or in the hypertrophy of a limb after 
injury to the opposite limb. The direct increased demand for 
work occasions the hypertrophy. Sometimes there appears to be 
a special tendency to hypertrophy, as is evidenced by the occur- 
rence of congenital or hereditary giant growth. Most of these, 
however, are instances of peculiar and abnormal development, 
rather than of hypertrophy, the latter being a condition developed 
pathologically in parts previously well formed. Disturbances of 
the nervous system may play a part in the development of some 
hypertrophies, but these influences are obscure. Continued conges- 
tion undoubtedly stimulates tissue-growth, but this element is the 
means whereby hypertrophy is effected rather than the original cause. 



PROGRESSIVE TISSUE-CHANGES. 



121 



Pathologic Anatomy. — Parts the seat of genuine hyper- 
trophy are uniformly increased in size. This is well seen in the 
condition termed giant growth, or gigantism, in which the bony 
framework and other tissues may be uniformly affected, the indi- 
vidual growing to excessive size. Sometimes local giant growth 
of the skeleton and external tissues is observed, as in the case 
of one member or a single finger. This has often been found in 
corresponding members on the two sides of the body. In certain 
cases termed hypertrophy, in which this designation is more 
or less justified, lack of uniformity in the increase of the organ or 
part affected causes irregular increase in size. 

Histologically, hypertrophy may he simple or true hypertrophy, 
and numerical (hyperplasia). In the former there is increase in 
the size of the individual cells ; in the latter the cells increase in 
number, though the individuals are not excessive in size, and 
indeed often smaller than the normal cells. In the hypertrophy 
of the uterus during pregnancy and of the heart-muscle in com- 
pensatory enlargement, simple hypertrophy predominates. Hyper- 
plasia is very commonly a factor in hypertrophy of any kind, but 
may be so strictly limited to one tissue of an organ, notably the 
connective tissue, that the term hypertrophy is in no way appli- 
cable. Between these extremes there are all grades of cases, in 
many of which it is difficult to determine whether the designation 
hypertrophy is applicable or not. In some cases the clinical desig- 
nation hypertrophic enlargement is used, though the condition is 
strictly one of hyperplasia of the connective tissue, with a ten- 
dency rather to atrophy than hypertrophy of the proper substance 
of the organ. Instances of this are hypertrophic cirrhosis of the 
liver, some cases of hypertrophy of the heart-muscle, etc. 

Pathologic Physiology. — Hypertrophy results from an 
increased demand upon an organ or member, and leads to increased 
functional capacity. Thus in the case of a diseased kidney the 
opposite kidney may be capable of compensating for the defi- 
ciency ; in the case of laborers the enlarged muscles may meet 
every demand made upon them. There are occasional instances 
of more or less genuine hypertrophy, resulting from diseased con- 
ditions, in which the excessive functional capacity causes marked 
disturbances, as, for example, in case of enlargement of the thy- 
roid gland. 

TUMORS. 

Synonyms. — New-growth, Neoplasm, Pseudoplasm. 

Definition. — In its broadest etymologic significance the term 
tumor designates an abnormal swelling in any part of the body. 
This definition, however, is not applicable to tumors in the ordi- 
nary sense. Inflammatory growths and collections, such as ab- 



122 



TEXT-BOOK OF PATHOLOGY. 



scesses, hyperplastic deposits, and the like, are excluded. Path- 
ologists, however, have always found it difficult to construct an 
accurate definition for tumors or to draw sharp lines of separation 
between them and the inflammatory or infectious swellings that 
occur in various diseased conditions. An attempt to establish an 
ultimate boundary -line is evidenced by the term autonomous new- 
growths applied by Thoma. This name is used to designate the 
supposed spontaneous origin of new-growths and their independence 
of ordinary causes, such as are recognized in the production of 
inflammatory outgrowths and the like. It cannot be said, how- 
ever, that tumors are causeless, and in the discussion of the eti- 
ology we shall have occasion to refer to certain definite factors 
known to aid in their production. It is true, however, that the 
growth of tumors is practically always out of proportion to the 
amount of local irritation or to the severity of other factors that 
may be conceived as playing some part in the etiology ; and in the 
great majority of cases the causes, whatever they may be, are 
obscure or unknown. A negative definition perhaps best suits for 
the delimitation of this term tumor. Thus we may exclude from 
the category of tumors all swellings in which some sufficient cause 
is discoverable, and include the apparently causeless growths 
among the true tumors. 

Etiology. — A great number of theories have been entertained 
to explain the causation of tumors. 

Among the older writers there was a disposition to attribute 
the occurrence of tumors to a constitutional dyscrasia, or a diseased 
state of the fluids of the body. This explanation, however, is 
based entirely upon speculation, and is most unsatisfactory in that 
the original dyscrasia is as difficult to explain as the tumor sup- 
posed to result from it. 

Recently a number of more elaborate theories have been con- 
structed that resemble this older one, in ascribing the growths to 
some form of disturbance of vital activity and of cell-proliferation r 
without explaining the cause of such disturbance. For example, 
we may refer to the theory that tumors result from a retrograde 
change in vital properties of certain cells, so that they tend toward 
the original properties of the germ-cells and multiply in a pur- 
poseless and indeterminate manner. Another theory would ex- 
plain the occurrence of new growths somewhat upon the basis of 
infection, assuming, instead of an exogenous infection with micro- 
organisms, an endogenous infection. This was suggested by the dis- 
covery of leukocytes within the tumor-cells. The author of this theory 
explains that in consequence of some thermic, chemical, or other 
irritation certain cells may become, so to speak, infectious, assum- 
ing the role of a sperm-cell and stimulating the adjacent cells to 
abnormal multiplication. Such theories, however, are entirely 
speculative, and leave the etiology as little settled as before. 



PROGRESSIVE TISSUE-CHANGES. 



123 



Virchow strongly advocated the theory of external irritation, 
and was able to cite numerous examples of tumors that had arisen 
in consequence of more or less definite causes. Thus in cases of 
carcinoma of the breast, in the epithelioma occurring on the lips 
in pipe-smokers, and in the epithelioma of chimney-sweeps, there is 
at times a definite history of unusual irritation, and the relation of 
cause and effect seems easily traceable. It must be admitted, 
however, that there is some further underlying cause which 
renders one individual liable to tumor-growth, while another is 
not thus predisposed, and though it is probable that some tumors 
owe their origin to irritation as the exciting-cause, all cases can- 
not be thus explained. 

Cohnheim advanced the interesting theory that defective devel- 
opment lies at the basis of tumor-formation. According to his 
theory, there are frequently small errors of development leading 
to the inclusion or misplacement of portions of the original blasto- 
derm in the midst of tissues derived from a different layer of the 
embryo. These inclusions or embryonic rests are independent of 
the function of the part in which they lie, and are assumed to be 
liable to subsequent sprouting with the consequent formation of 
tumors. There is evidence that this theory contains a certain 
measure of truth, and some tumors, as, for example, certain 
ovarian growths, tumors of the parotid region, and others, seem to 
originate in this way. The theory, however, is not by any means 
universally applicable, and it does not explain the eventual pro- 
liferation of the embryonal rests that had previously remained 
dormant. 

Recently an infectious character has been ascribed to malignant 
and benign growths, and there is no doubt that in certain respects 
tumors resemble infectious processes of definitely ascertained 
kinds. Their effect upon the general health and their tendency 
to metastasis are very significant facts. Notwithstanding this, 
however, the proof of the infectious nature of tumors remains to 
be furnished. . Careful investigations haxe excluded bacteria in 
the case of most forms of tumors, but in the case of certain sarco- 
mata (lymphosarcoma) it seems possible that bacteria are the im- 
mediate factors. In carcinomata and other epithelial new- 
growths, as well as in sarcoma, certain forms of intracellular 
animal parasites (see Animal Parasites) have been described, 
though the nature of these bodies still remains in doubt ; and 
recently the theory is gaining ground that blastomycetes are active 
in the production of tumors. Upon the whole, though it must 
be admitted that the infectious nature of tumors is probable, the 
actual proof still remains wanting. In experiments upon ani- 
mals and upon mail it has been possible in a few cases to demon- 
strate inoculability. The significance of this fact, however, must 
not be overestimated, and it certainly cannot be assumed with- 



124 



TEXT-BOOK OF PATHOLOGY. 



out further proof that this evidences the infectious nature of the 
growths. 

Predisposing Conditions. — Whatever may eventually prove to 
be the immediate cause of tumors, it is certain that predisposing 
causes are often of great importance. The occurrence of certain 
forms of tumors in persons of advanced age and in persons whose 
vitality has been reduced by disease gives evidence that a consti- 
tutional predisposition is sometimes requisite for the formation of 
the new growth. The nature of this vital defect has sometimes 
been speculated upon, and retrograde vital metamorphosis of the 
cells or other like changes have been assumed to occur. These 
theories, however, are purely speculative. In some cases there is 
evidence of a family predisposition, and heredity was formerly 
regarded as of great importance. While this element cannot be 
entirely denied, it has certainly been over-estimated. 

The Structure of Tumors. — In their histologic structure 
tumors do not differ absolutely from healthy tissues. In all cases 
they conform more or less with the structure of some one or more 
tissues. The cells composing tumors invariably represent some 
one or several types of normal cells, though they may differ in 
being larger or smaller than the normal cells, or in being of 
embryonal or undeveloped character. In the arrangement of the 
cells, however, there is a notable difference, and tumors may be 
described as being atypical proliferations as far as their organic or 
tissue arrangement is concerned. The orderly disposition of cells 
and stroma or intercellular substance seen in the normal tissues 
and organs is wanting, particularly in the tumors in which organic 
arrangement is simulated. There may be in some cases entirely 
typical glandular acini, but the relation of these to each other 
and the absence of regularly disposed excretory ducts render the 
tissue as a Avhole atypical. 

The structure of tumors is always closely related to that of 
the tissue from which it springs, a primary tumor invariably grow- 
ing in a part in which there is tissue of the type simulated by the 
tumor, and it is from this tissue, doubtless, that the tumor takes 
its origin. A connective-tissue growth invariably springs from 
a part in which connective tissue of some form has pre-existed, 
and epithelial growths from a part in which there has been 
epithelium. Metaplasia, or the transformation of one variety of 
tissue into another variety, with the production of a tumor, does 
not occur. This statement, though applicable also to secondary 
tumors, is sometimes difficult of demonstration from the fact that 
the secondary growths take origin from cells transported to the 
seat of growth from a primary tumor, though not normally found 
in the part in which the secondary tumor has arisen. The occa- 
sional discovery of a primary tumor in a locality in which the 
form of tissue composing the tumor does not occur may be ex- 



PROGRESSIVE TISSUE-CHANGES. 



125 



plained upon the assumption (based on some actual demonstra- 
tions) that embryonic rests had been deposited at the seat of the 
tumor by faulty development. 

The' Shape of Tumors.— This depends to a large extent 
upon their manner of growth, their situation, and the influence of 
surrounding parts. We may distinguish, first of all, between 
circumscribed and infiltrating growths. The former may be of 
various shapes, but are distinguished by their sharp delimitation 
and often by the existence of a distinct capsule ; the latter are 
indeterminate, and the extent to which they involve the healthy 
tissues cannot be accurately determined. Circumscribed tumors 
usually grow centrally or in an expansive manner, the new cells 
being produced in the interior and gradually pushing the older 
parts outward toward the surrounding tissues. The infiltrating 
growths are eccentric in development, and may result from a 
gradual extension of parts of the periphery of the original growth 
or by the development of secondary nodules in the neighborhood 
which become confluent with the original mass. Of the circum- 
scribed growths we may distinguish small nodules of spherical or 
ovoidal form buried in the substance of the tissue or projecting 
from some surface as more or less hemispherical elevations. These 
may be large or small, and the terms miliary, tubercular, nodular, 
and the like are employed to designate the individual grades. 
When a tumor projects from the surface in such a manner that the 
projecting part is larger than the part between the projection and 
the surface of the body or the organ involved, the term fungiform 
or fungoid tumor may be applied, w r hile in the cases in which the 
new growth is attached by a more or less narrow pedicle the name 
polyp or polypoid tumor is applicable. Wart-like growths are 
known as verrucose or papillary tumors, and those in Avhich a dis- 
tinct cauliflower-form is developed are called dendritic. 

The Number of Tumors. — Primary tumors are usually 
solitary at their onset, though examples of multiple primary 
growths, such as carcinoma involving both breasts simultaneously, 
or simultaneous appearance of carcinomata or sarcomata in differ- 
ent parts of the mucous membrane or elsewhere, may be observed. 
In these cases it is often likely that there was a single tumor at 
the very onset, with secondary growths originating before the 
primary growth had reached any considerable magnitude. Primary 
benign tumors are usually solitary, but sometimes may be found 
in considerable number, and there may be enormous numbers 
scattered in various parts of the body. Thus in cases of multiple 
enchondromata or multiple fibromata the number may from the 
first be very great. 

Secondary tumors are usually multiple. In most cases the 
number of nodules found post-mortem or during life is considerable, 
and sometimes they are so numerous that large portions of the 



126 



TEXT-BOOK OF PATHOLOGY. 



body may be literally studded with new-growths. This is seen 
very well in the secondary sarcomatous or carcinomatous nodules 
involving the peritoneum and the other serous surfaces, in which 
cases the degree of involvement is simulated only by that seen in 
miliary tuberculosis. 

Pathologic Physiology. — In most cases tumors take no part 
in the functional life of the part in which they occur or of the in- 
dividual. What influence they may bear to the general metabolism 
is as yet practically unknown. Cases, however, are recorded in 
which large lipomatous or other tumors have been found to suffer 
practically no change, while the individual in whom they occurred 
was undergoing progressive emaciation from starvation. That 
there is a certain amount of function, however, in some cases is 
shown by the fact that biliary pigment is detected in the cells in 
certain carcinomatous tumors of the liver, or abortive milk-forma- 
tion in cancers of the breast. It may be that the want of proper 
organic arrangement, and particularly the lack of excretory ducts, 
accounts for the lack of function ; but whatever the cause, it is 
certain that as a rule the functional activity is practically nil, or at 
all events perverted. The occurrence of large quantities of 
glycogen in certain tumors is perhaps of interest as indicating an 
attempt at functional activity, but is more probably significant 
only of active proliferation. With very few exceptions it may be 
said that tumors are entirely parasitic, living at the expense of the 
organism and contributing nothing to its development or nutri- 
tion. 

Certain tumors disturb the general health. This result may be 
due to secondary degenerative or inflammatory changes dependent 
upon lack of nutrition or upon irritation and bacterial infection ; 
or to obscure causes connected with the tumor-growth itself. The 
progressive cachexia of carcinoma is still unexplained, though in 
some cases hemorrhage and interference with organic function 
play a part. 

Tumors may be classified as benign or malignant. The former 
do not affect the general health of the patient in any notable de- 
gree, and are dangerous mainly by reason of the pressure they may 
exert on vital structures or the secondary changes (hemorrhages, 
softening, suppuration) to which they are liable. Malignant 
tumors generally disturb the general health from the first, and, in 
addition, tend to recur after removal and spread to other parts of 
the body (by direct invasion or by metastasis through the circu- 
lation or lymphatic channels). The terms primary and secondary 
tumors refer to the original and the metastatic growths respectively. 

Classification of Tumors. — No very satisfactory classifica- 
tion is possible at the present time, and it is unlikely that any will 
be constructed until more definite knowledge regarding the etiology 
is obtained. The older classifications were based upon the shape, 



PR GRESSIVE TISSUE-CHANGES. 



127 



the physical properties, or the nature (whether destructive or 
harmless) of various forms. Virehow offered a classification 
based on the histology (histogenetic classification) ; others have 
grouped tumors according to the embryologic derivation of the tis- 
sues from which the new-growths originate or of the tissue com- 
posing the tumor. It is perhaps wisest to attempt no classification 
of any kind, and in the following sections I have arranged the 
various tumors according to their histologic characters without 
attempting to establish groups. 

FIBROMA. 

Definition. — A fibroma is a tumor composed of connective- 
tissue cells and fibers resembling those seen in fibrillar tissue. 

Etiology. — The causes of fibroma are as obscure as are those 
of tumors in general. There are many facts, however, which 
point to the importance of irritation or injury as exciting causes. 
Among these may be mentioned the development of a peculiar 
form (keloids) in scar-tissue and the resemblance of these tumors 
to spontaneous fibromata, and the appearance of fibrous nodules in 
the skin at points of friction or definite pressure or in places irri- 
tated by discharges. 

It is impossible to draw sharp lines between fibromata and 
hyperplasias of connective tissue following irritation. In the 
skin and superficial tissues there occur hyperplastic connective- 
tissue processes, constituting elephantiasis, which in some cases 
are distinctly the result of irritation and in other cases seem 
purely spontaneous. The elephantiasis of tropical countries, often 
due to occlusion of the lymphatic channels by filaria?, and the 
thickening of the skin and adjacent connective tissue of the legs 
around old ulcerations or eczematous areas, are instances in which 
distinct irritation is the cause. On the other hand, congenital 
elephantoid conditions of the skin are seemingly spontaneous or 
causeless, and some of the cases in later life have the same char- 
acteristic. The diffuse hyperplasias of the viscera, though often 
distinctly inflammatory, may appear without adequate discover- 
able cause, and, according to the view of some authorities, are 
to be looked upon as diffuse fibrosis or fibromatosis, rather than 
as inflammatory conditions. In ordinary cases of cirrhosis of 
the organs the connective-tissue growth is entirely diffuse, but 
thickenings may occur in certain situations, and the resemblance 
to tumor-formation is then much more striking:. This is sometimes 
the case in the liver, but particularly in the kidneys. In the 
breast there are cases in which no dividing-line can be drawn 
between chronic interstitial mastitis and fibroma. The micro- 
scopic appearances are practically identical. A distinction, if any 
can be made, is based upon the nodular character and spontaneous 
origin in the one and the opposite conditions in the other. 



128 



TEXT-BOOK OF PATHOLOGY. 



Appearance. — The naked-eye appearance of fibromata is 
usually quite characteristic. The tumor may be hard (Fig. 38) 




Fig. 38.— Hard fibroma (Warren). 



or soft (Fig. 39), according as it resembles loose or dense con- 
nective tissue in structure and according to the amount of 




Fig. 39. — Soft fibroma of the subcutaneous tissue. 



edematous liquid or associated myxomatous degeneration of the 
intercellular substance. The growth is more or less rounded and 
usually enclosed in a distinct capsule. In the substance of organs 
it is spherical or tuberous, and w T hen near the surface projects more 
or less. When it springs from a mucous or serous membrane or 
from the skin the weight of the tumor may gradually lead to a 
polypoid formation. Some of the fibromata of the skin are arbo- 
rescent or dendritic in form, and keloids are frequently irregular 
or star-like in outline. The rounded and encapsulated tumors 
may be lobulated, though more frequently they occur in a uniform 
mass. 

Seats. — The points of origin from which fibroid tumors arise 



PROGRESSIVE TISSUE-CHANGES. 



129 



are very numerous, though they always spring from pre-existing 
connective tissue. Among some of the more common localities 
may be mentioned the subcutaneous connective tissue, the sub- 
mucous tissue, the periosteum of bones, tendons and tendon- 
sheaths, and the fibrous covering of nerves. Of the internal 
organs, the uterus, the ovaries, the kidneys, and heart-muscle are 
the most important. Less frequently fibromata are found in the 
serous membranes of the chest and abdomen or of the central ner- 
vous system. The fibroids of the skin, the uterus, the nerves (see 
Neuroma), and the mucous membrane of the nose are the most 
important. 

The mammary gland presents several interesting forms of in- 
flammatory or fibromatous new-growth. First, there is a diffuse 
form of interstitial mastitis in which the entire breast becomes 
indurated ; this is distinctly inflammatory. In other cases nodular 
or lobular areas of thickening occur, and in these the evidences of 




Fig. 40.— Intracanalicular fibroma (Perls). 



inflammatory action are sometimes obscure or wholly wanting. 
Some of these are certainly instances of true fibroma {fibroma 
mammae nodulum). In still another group of cases the fibromatous 
proliferation of the connective tissue projects into the tubules and 
acini of the gland, pushing the epithelium before it and sometimes 
sprouting or proliferating in polypoid form within the tubules. 
The gland in such cases may present a striking macroscopic appear- 
ance on section. Numerous cystic formations may be visible with 
projecting dendritic formations within, causing an appearance 
somewhat like that of a section through a cauliflower (Fig. 40). 
Microscopically the proliferations of the connective tissue between 
the tubules and projecting within the tubules constitute the 
characteristic features. The term intracanalicular fibroma has 
been given to such cases. Obstruction of the tubules in certain 

9 



130 



TEXT-BOOK OF PATHOLOGY. 



areas may lead to very marked cystic distention. Combinations 
with sarcoma are frequent. 

Structure. — The definition explains the structure of fibro- 
mata. On section through the body of the tumor the fibrous 
nature may be revealed by a distinct concentric or radiating 
striation, particularly in the case of hard fibromata. The softer 
varieties are much less likely to present this feature. The color 
is usually gray or whitish, and may be glistening when there is 
mucous degeneration, or yellow in the case of associated lipoma. 
Microscopically a striking feature is the connective-tissue cell, 
which is star-like and branching in the softer tumors, and com- 
pressed, spindle-shaped, or elongated in the case of the hard 
varieties. The intercellular substance is composed of a fibrillar 
network and homogeneous or granular material traversed by thin- 
walled blood-vessels, ofttimes having merely an endothelial coat. 
Cavernous dilatation and rupture of the vessels may cause a dis- 
tinct hemorrhagic appearance of the section ; but such conditions 
are rare. 

In some cases embryonal round cells may be abundant and a 
distinct sarcomatous transformation of the tumor may occur. 
This, however, is rare. In other instances, as has already been 
remarked, myxomatous tissue may be conspicuous, and all grades 
of transformation from a pure fibroma to a pure myxoma may be 
met with, especially in the case of soft fibroma. Fatty degenera- 
tion of the cells and lipomatous infiltration or associated lipoma 
are also frequent. These forms, the myxomatous and lipomatous, 
are particularly frequent in the submucous and subcutaneous con- 
nective tissues. Calcareous degeneration occurs in large fibrom- 
atous tumors, particularly in those of the uterus, and very rarely 
true ossification has been reported. Less commonly association 
of fibroma with other forms of tumor-growth is found. Among 
these the combination of fibroma with leiomyoma is usual in the 
uterus. 

Nature. — Fibroma is essentially a benign tumor, though 
recurrence occasionally takes place after removal, this being par- 
ticularly the case with keloids and some of the polypoid growths 
of mucous membranes. In some of these instances there is 
undoubtedly a resemblance to sarcoma, if not actual sarcomatous 
transformation. As a rule, fibroid tumors are destructive only in 
so far as they are capable of producing mechanical injury by press- 
ure. The growth of the tumors is usually exceedingly slow. 

MYXOMA. 

Definition. — Myxoma is a tumor composed of connective- 
tissue cells and an intercellular substance containing mucoid 
material in more or less abundance. The gelatinous substance of 



PE GRESSIVE TISS UE- CHA XGES. 



131 



Wharton in the umbilical cord and the vitreous humor of the eve 
are normal types which myxomata resemble in their structure. 

Etiology. — The causes and the nature of myxomata are 
practically the same as those of fibroma, and intermediate forms 
make it difficult to draw a sharp line between the two. 

Appearance. — A typical myxoma is a soft, more or less 
flabby growth enclosed by a capsule, and having a rounded out- 
line. It may project from the surface of the body or of an organ 
as a hemispherical elevation, or may hang by a narrowed pedicle 
in the form of a distinct polyp. The latter is frequent in the 
mucous membranes, but may occur in the skin as well. Some- 
times the tumor is lobulated, and the lobules may be visible or 
may be easily felt. Occasionally lipomatous growths are diffuse, 
having no capsule and marked by no definite limits. 

Seats. — Among the common situations are the subcutaneous 
and submucous tissues and the connective tissues of certain organs, 
notably the mammary glands. They may occur along the course 
of nerves, in the brain or the spinal cord. The tumor may be 




Fig. -il.— Myxoma, showing stellate cells separated by a gelatinous (mucoid) 
intercellular material. 



solitary, or, like fibroma, may be met with in numbers. Congeni- 
tal myxoma has frequently been found. 

Structure. — Microscopically the characteristic features are 
stellate or spindle-shaped connective-tissue cells which lie within 
a matrix of myxomatous material (Fig. 41). The latter is homo- 
geneous or slightly granular, and somewhat refractive to the light, 
giving the surface a glistening quality. The cells themselves may 
be entirely normal young connective-tissue cells, or they may present 
evidences of fatty degeneration. Round granulation-tissue cells 
are met with in some instances, either scattered through the tumor 
or in certain areas, and may be so abundant as to justify the term 



132 



TEXT-BOOK OF PATHOLOGY. 



myxosarcoma. The vascular supply is usually poor, and the 
blood-vessels resemble those of fibroma in being only partially 
developed. Association with fibroma and lipoma is frequent. 
Cartilaginous tissue may be found in myxomatous tumors of the 
parotid gland or testicle, and in these cases the myxomatous 
portion is rather an association than a degeneration of the original 
chondroma. Myxomatous degeneration of chondromata, osteo- 
mata, fibromata, and sarcomata is, however, a frequent occurrence. 

Nature. — Myxoma is benign like fibroma, but recurrence is 
not infrequently observed, and in a few instances metastasis has 
been reported. It is difficult, however, to assert the absence of 
sarcomatous change in these instances. The growth of myxomata 
is slow. 

LIPOMA. 

Definition. — A lipoma is a tumor composed of fatty tissue 
like that of the normal subcutaneous tissue. The epiploic ap- 
pendages of the intestines are the normal type which lipomata 
resemble. 

Etiology. — There seems to be a tendency, consisting perhaps 
in some derangement of the trophic nervous system, to the growth 
of these tumors. It is difficult at times to draw a sharp line be- 
tween circumscribed lipomata and diffuse fatty growth. Localized 
fatty or myxolipomatous accumulations in myxedema and a curious 
and apparently causeless deposit of fatty tissue sometimes observed 
in the subcutaneous tissue of the neck in men, represent the bor- 
der-line between lipomata and ordinary obesity. Some individuals 
have a marked liability to constant overgrowth of fat in different 
parts of the body, and the term " lipomatosis " is not inapplicable. 
This fatty growth does not apparently depend upon the character 
or quantity of food, nor even upon sedentary life in some cases, 
but rather on an obscure tendency to adipose accumulation. 
Traumatism seems to play no part, though fatty infiltrations are 
prone to occur around areas of injury or disease, and in degenerated 
organs. 

Appearance. — Lipomata are usually circumscribed and en- 
capsulated tumors having a lobulated character, the latter being 
due to septa of connective tissue. On the surface of the body 
they appear as somewhat hemispherical elevations which may 
reach enormous proportions. Rarely they become polypoid. In 
the interior of the body, as, for example, when they arise in 
the submucous or subserous connective tissue, they are very 
frequently, though not always, polypoid. Sometimes they be- 
come detached and may be retained in one of the cavities of 
the body as free bodies. On section the appearance is that of 
fatty tissue, though in some cases it is more firm from the associa- 
tion of fibrous tissue, and in other cases less firm from the nature 



PROGRESSIVE TISSUE-CHANGES. 



133 



of the fatty tissue itself or from associated myxomatous change. 
Lipomata may be solitary tumors, or there may be many. As a 
rule, they appear in adult years or middle life, but congenital 
lipomata are not very rare ; and occasionally they are found to 
begin in childhood. 

Seats. — Among the situations in which lipomata occur the most 
common are the subcutaneous fatty tissue of the back, shoulders, 
buttocks, or limbs, the submucous, and the subserous tissues. 
They may arise either in the normal fatty tissue or in connective 
tissues in which fat is not normally present. Some authors, how- 
ever, deny the possibility of lipomata arising excepting from pre- 
existing fatty tissue. Of the organs,* the mammary gland and the 
kidney are most frequently involved. 

Structure. — Microscopically lipomatous tumors resemble the 
normal fat. It is notable that the cells are larger — that is, con- 
tain more oil — than the normal fat-cells, and this is strikingly the 
case in some instances, but is not always demonstrable. The 
vascular supply is about the same as in normal fat, though occa- 
sionally large vessels with thin walls are seen. Associated myx- 
omatous or fibrous change may cause a variation of the microscopic 
appearance. 

Lipomata may undergo softening from necrosis, but more fre- 
quently become calcareous in part or completely. 

Nature. — This is the most benign form of tumors. Recur- 
rence after more or less complete removal does, however, at times 
occur. A lipoma is dangerous only from its weight or position. 
It does not contribute to the support of the system in case of 
starvation. 

XANTHOMA. 

Definition. — This term is applied to two possibly distinct though similar 
forms of new growth. The xanthoma vulgare occurs most frequently in 
the eyelids and may be confined to that situation. The growth appears in 
the form of flat elevations of a yellow color. Generalized xanthoma begin- 
ning about the eyes is less frequent. Xanthoma diabeticorum is a similar 
affection of diabetic patients. It occurs at a more advanced age, is more 
distinctly inflammatory, the masses are more rounded, and the eyelids and 
face are rarely affected. 

Structure. — The histology of xanthoma is that of modified fatty tissue. 
It resembles embryonal adipose tissue, and there is usually more or less 
round-cell infiltration as well. Some authors regard the latter as a tendency 
to sarcomatous change ; others look upon it as inflammatory. 

Nature. — Xanthoma is eminently benign. The diabetic form is subject 
to sudden and apparently causeless involution. The ordinary form may 
similarly subside, though much less commonly. 



134 



TEXT-BOOK OF PATHOLOGY. 



CHONDROMA. 

Definition. — A chondroma is a tumor composed largely or 
entirely of cartilage. It is difficult to draw a sharp line between 
outgrowths of cartilage from existing cartilage or bone due to irri- 
tation from definite and independent tumor-like growths. A 
group of cases of intermediary character is that including carti- 
laginous nodules formed in tendons of muscles subjected to fre- 
quent irritations, as in the deltoid muscles in soldiers carrying 
heavy arms, and in the adductor muscles of the thigh in horse- 
back riders. In these cases normal connective tissue seems to be 
directly transformed into cartilage, though the influence of irrita- 
tion is undoubted. 

etiology. — A congenital disposition, sometimes hereditary, is 
unquestionably present in certain cases. Virchow maintained that 
chondromata often spring from remnants or islands of cartilage 
left in abnormal situations, as in the midst of bone, as the result 
of imperfect fetal development. The same explanation would 
account for parotid chondromata on the assumption that parts of 
the branchial arches are misplaced and remain in the substance of 
the parotid gland. 

Irritation has been referred to. Direct traumatism is some- 
times the cause of cartilaginous outgrowths from bone, particularly 
when fractures have occurred. 

Appearance. — Two distinct forms may be considered, and 
these are somewhat different in appearance. They are (1) carti- 
laginous outgrowths, ecchondroses or ecchondromata, and (2) 
independent cartilaginous tumors, or chondromata proper. 

Ecchondromata present themselves as rounded or somewhat 
irregular outgrowths from bones or cartilages. Sometimes they 
are wart-like in form and may occur in rows or groups. They 
may be firmly attached, or may be loosely united to the bone. 
The most frequent and the most characteristic are the outgrowths 
in the articular cartilage occurring in chronic arthritis, particularly 
in rheumatoid arthritis. Occasionally they become detached after 
their formation, and in the joints may thus become free bodies. 
The large chondromata are generally distinctly lobular or irregular 
in outline. 

Chondromata springing from the inner surface of bones (pos- 
sibly originating from the marrow itself) may grow uniformly by 
repeated or constant proliferation and lead to globular swellings 
of the affected bones (Fig. 42). The true bony covering becomes 
more and more thin until it may actually perforate. 

The true chondromata are usually rounded bodies ; they pre- 
sent lobular irregularity when they reach considerable size, the 
lobules being separated by connective tissue. 

All forms are hard, though secondary softening may occur. 



PROGRESSIVE TISSUE-CHANGES. 



135 



In cases in which association of mucous, sarcomatous, or other 
soft tissue is present the consistency is correspondingly less. In 
some cases central softening leads to cystic formation. The 
liquid in the cyst is more or less turbid and occasionally san- 
guinolent. 

Seats. — Ecchondroses and chondromata, for the most part, 
take their origin from bone, cartilage, or periosteum. In some 
cases, however, they originate in connective tissue, as that of the 
tendons, by a process of cartilaginous metaplasia. Cartilage- 




Fig. 42.— Chondroma of the thumb (Warren). 



tumors are met with in some of the glandular organs, notably the 
parotid gland, testicle, and ovary ; and rarely they occur in the 
lungs, especially at the root and springing from the peribronchial 
cartilages. 

Ecchondroses are most frequent about the long bones, as those 
of the extremities, and particularly at the epiphyseal attachments. 
They are not at all infrequent, and may reach considerable propor- 
tions in these situations. Situations of great clinical importance 
are the interpubic and occipitosphenoidal junctions. In the former 
situation ecchondroses projecting inward may interfere seriously 
with labor, and in the latter place cartilaginous outgrowths may 
penetrate the dura and exercise injurious compression on the brain. 
Allusion has been made to the ecchondroses of the joints in 
arthritis. 

Chondromata proper may occur in the neighborhood of bones, 
in the muscles and tendons near their bony attachments, and in 
the organs mentioned, but in the last situation are rarely pure, 
myxoma being the most frequent associate. 

Structure. — Chondromata resemble hyaline, fibrous, or elastic 
cartilage, the first-named being much the most frequent. The 
tissue differs from normal cartilage in the fact that the cells are 
frequently without capsules and are much less regularly arranged 



136 



TEXT-BOOK OF PATHOLOGY. 



(Fig. 43). The intercellular substance is more abundant and is 
frequently gelatinous, mucoid, or fibrous, and not rarely the differ- 
ent types of cartilage occur within narrow limits. Association 




Fig. 43.— Chondroma of the hyaline type. 



with myxoma and sarcoma, or both, is common, especially in the 
parotid and testicles, the proportion of the several ingredients 
varying greatly. Tumors of this kind are spoken of as mixed 
tumors. Calcification and true ossification are not infrequent, par- 
ticularly in cartilage-tumors intimately connected with bone. The 
term osteochondroma is applied in such cases. The name osteoid- 
chondroma is applied to chondromata in which the intercellular 
substance is trabecular in arrangement, suggesting bone-structure, 
but in which actual ossification has not occurred. Such growths 
are met with about the bones and, as a rule, spring from the 
periosteum. 

Degenerative changes are frequent. Myxomatous degenera- 
tion may occur, though myxoma is more frequent as an association 
than as a degeneration. Softening may occur in the center of the 
mass, and may lead to cyst-formation, this being particularly com- 
mon in the myxochondromata. Growths of this kind are fre- 
quently quite vascular and hemorrhages into the cysts may occur. 
Eventually such cases may show scarcely any cartilage-cells, a few 
being perhaps detected in some part of the cyst-wall. A single 
Jiard lump may be left at one side of the cyst, the rest of the 
tumor having softened. 

Nature. — Chondromata are essentially benign, and are danger- 
ous only through the pressure they exert. Removal of a part of 
the tumor may have a beneficial influence in causing calcification 
of the remainder. Metastasis may undoubtedly occur in pure 



PROGRESSIVE TISSUE-CHANGES. 



137 



chondromata through transportation of particles in the circulation. 
Such cartilaginous emboli have often been demonstrated. The % 
secondary growths are most frequent in the lungs. Metastatic 
chondromata are, however, more frequently choridrosarcomata 
than pure chondromata. 

OSTEOMA. 

Definition. — An osteoma is a tumor composed of osseous 
tissue. Osteomata are closely allied to cartilaginous tumors, and 
frequently transformations occur. 

Etiology. — The same difficulty is experienced in distin- 
guishing inflammatory outgrowths or exostoses from true bony 
tumors, as in the case of cartilaginous growths. Enlargement 




Fig. 44.— Exostoses of the elbow-joint. 



of the facial bones in leontiasis ossea, of the bones of the extrem- 
ities in acromegaly and hypertrophic pulmonary osteoarthrop- 
athy, and ossifications of the muscles in myositis ossificans, are 
instances of border-line conditions separating true tumors from 
inflammatory hyperostoses. Irritation and traumatism undoubt- 
edly play a part in the etiology, even in neoplasms unattached to 
the bone, and in the case of bony outgrowths injury is generally 
the immediate cause. An underlying predisposition undoubtedly 
exists, and explains the occurrence of congenital multiple bony 
tumors. 

Appearance. — Two forms may be distinguished, as in the case 
of chondromata : (1) outgrowths or exostoses and osteophytes, and 
(2) the osteomata proper, or heteroplastic osteomata. Exostoses 
and osteophytes are distinguished one from the other by their 
shape and appearance rather than by any essential difference. The 
former are direct outgrowths of more or less wart-like character ; the 
latter are more extensive and present the appearance of bony deposits 
upon bones, and are less closely attached (Fig. 44). In both forms 



138 



TEXT-BOOK OF PATHOLOGY. 




the surface of the growth is irregular, nodulated, or wart-like 
(Fig. 45). The consistency is that of bone, and the size varies 

from that of small outgrowths to 
masses as large as a fist. On 
, s j * f section two forms may be dis- 

tinguished ; the hard or osteoma 
durum, and the soft or osteoma 
spongiosum. Sometimes the sub- 
's. ■'■> stance of the tumor is exceedingly 
m 1 2 ^ P-n ■^Bb^ dense, and the term osteoma ebur- 
^mmjQnnmS neum is applied. 

The heteroplastic osteomata, or 
those separated from the bone, are 
more rounded and, when of con- 
siderable size, usually nodulated 
and lobulated. In the serous 
fig. 45,-osteoma^the lower jaw mem branes they occur as flat 

bonv plates. 

Seats. — Osteomata spring from the bone or cartilage, or from 
connective tissue near the bones. More rarely they arise in other 
connective tissues, in the serous membranes, or in certain organs, 
notably the testicle and parotid gland. 

Osteomata connected with bones are most frequent about the 
epiphyses, at the attachments of muscles, or at the seat of old 
fractures from which abundant callous has been deposited. The 
skull-bones may be affected on the outer or inner surface, and 
often an elevation is noted without and within at the same spot. 
A form of clinical importance is that in which exostoses occur on 
the inner aspect of the metatarsal bone of the great toe from com- 
pression of tight shoes. In the maxillary bones osteomata may 
originate about the roots of malformed teeth. In cases of accumu- 
lation of cement-substance beginning at the neck of the tooth the 
term dental osteoma is applied ; these are strictly comparable to 
osteomata. In cases in which proliferation of the dental pulp 
has occurred the term odontoma is applicable, and the tumor is not 
of osseous character. The bony growths sometimes seen in the 
serous surfaces nearly always arise in areas in which there has 
been thickening from chronic inflammation. They are most fre- 
quent in the dura mater of the brain, particularly the falx cerebri ; 
though the membranes of the cord, the pleura, or pericardium may 
be involved. 

Structure. — Microscopically osteomata resemble more or less 
accurately bone-tissue. They vary, however, in different areas, 
and mixtures of cartilage with bony tissue are frequent. Second- 
ary degenerative changes (softening) may occur and association 
with tumors of other character are not infrequent (chondroma, 
myxoma, fibroma, sarcoma). 



PROGRESSIVE TISSUE-CHANGES. 



139 



Nature. — These growths are eminently benign, do not recur, 
and do not give metastasis. Their situation sometimes makes 
them troublesome or dangerous. 

LYMPHANGIOMA. 

A lymphangioma is a tumor composed of dilated lymph-vessels 
or lymph-spaces; more frequently the latter. It is difficult to 
separate dilatations of lymphatic channels due to obstruction from 
hyperplastic processes. Congenital enlargements of certain parts 
are met with which seem entirely dependent upon the abnormal 
development of the lymph-spaces. These constitute the condition 
called elephantiasis congenita mollis, in which the subcutaneous 
tissues are boggy or edematous, and even distinct cystic formations 
occur. Congenital cystic hygroma is an instance of dilatation of 
the lymph-spaces. Congenital enlargement of the tongue, termed 
macroglossia ; of the lips, mdcrocheilia ; and of the skin, ncevus 
lymphaticus ; are other instances of the same process. In all of 
these, in addition to the dilatation of the lymphatic spaces, a 
marked proliferation of the connective tissues as well as the 
muscle (in the case of the tongue) is striking ; but the process in 
all probability originates as a dilatation of the lymph-spaces. 
The terms lymphangioma cavernosum and cavernoma, lymphaticum 
have been suggested for these cases of dilatation of the lymph- 
spaces. On staining with silver-salts the endothelial lining of the 
spaces may be readily demonstrated. Actual enlargement and 
varicosity of existing lymphatic vessels may occur, but is ex- 
tremely rare in the form of circumscribed growths ; it is met with 
more frequently in association with general processes, such as ele- 
phantiasis. The bursting of dilated lymphatics may lead to 
lymphorrhea or external discharge of lymph when the process 
involves the skin, or to effusions of lymphatic character when the 
serous cavities are involved. Chylous pericarditis, pleuritis, and 
ascites are thus produced. Rupture of dilated lymphatics along 
the urinary tract (kidney or bladder) occasions chyluria. Lymph- 
angioma is a benign process in the pathologic sense. 

HEMANGIOMA. 

Definition. — An hemangioma, or angioma as it is more fre- 
quently called, is a tumor-like formation composed principally of 
blood-vessels. Strictly speaking, many of these are not tumors, 
being merely localized dilatations and elongations of pre-existing 
blood-vessels. Some, however, represent actual proliferations. 
Two varieties may be described, that in which the blood-vessels 
are merely distended (angioma teleangiectaticum), and that in which 
there are enlarged spaces lined with endothelium (angioma cavern- 
osum or cavernoma). In many tumors the blood-vessels are some- 
what enlarged ; these are spoken of as teleangiectatic. 



140 



TEXT-BOOK OF PATHOLOGY. 



Etiology. — Congenital malformation certainly plays some 
part in certain cases, as the frequency of hemangiomata in the 
new-born and particularly at the junction of the branchial arches 
would indicate. Injury, however, and mechanical causes gener- 
ally also play a part, and pre-existing disease, particularly fibroid 
inflammatory processes, may contribute to the subsequent dilata- 
tion and proliferation of the vessels (see below). 

Appearance and Seats. — The angioma teleangiectaticum 
may involve only the arterioles and capillaries, and in this case a 
bright-red color is observed. The tumor appears as a spot on the 
surface of the skin, more or less sharply outlined from the sur- 
rounding tissue. It is not elevated and has the same consistency 
as the healthy parts. Usually it occurs as a multiple condition, 
and the larger are often surrounded by smaller spots. The skin 
is the favorite seat ; but the subcutaneous tissue and sometimes 
the mucous membranes are involved. Less commonly the veins 
are implicated, when a dark-red color is observed (port-wine- 
stains). 

If a circumscribed portion of the circulation is uniformly in- 
volved, the vessels thicken and elongate, and a peculiar form of 
hemangioma results. In these cases the arteries are greatly thick- 
ened and tortuous, and form bunches under the skin, suggesting to 
palpation a bundle of earth-worms ; while the surface of the skin 
presents peculiar irregular elevations without of necessity any 
change of color (aneurysma racemosum seu cirsoideum). This is 
not infrequent in the scalp. A similar condition of the vessels is 
observed in the varicosity of the legs, labia, or other parts. It is 
most frequent in the hemorrhoidal veins, constituting the ordinary 
hemorrhoids. (These conditions will be more fully described in 
discussing the diseases of the vessels.) 

Cavernous angiomata present themselves as more distinctly 
tumor-like formations of dark venous color, involving the skin or 
subcutaneous tissues, the retrobulbar tissue of the eye, the mucous 
membranes of the nose or pharynx, and certain organs, as the 
mammae, the kidney, the spleen, but particularly the liver. Like 
the other variety, they may be congenital, but more frequently 
arise in later life, especially that of the liver, which is most com- 
mon in old persons. The appearance is that of a more circum- 
scribed tumor, sometimes showing a distinct capsule and varying 
in consistency with the degree of distention of the blood-spaces. 
In the skin it projects slightly from the surface (ncevus promi- 
nens) ; in the liver the tumor does not project. 

Structure. — The definition explains the structure in general. 
The blood-vessels of teleangiectatic angiomata may be simply di- 
lated capillaries with a lining of endothelium and a fibrous outer 
coating. More commonly the vessels are considerably thickened 
and held together by a reticular connective tissue. In rare in- 



PROGRESSIVE TISSUE-CHANGES. 



141 



stances the vessels are so closely packed and the walls so thickened 
that when the blood is removed the appearance is not unlike that of 
the tubules of a sweat-gland. The cavernous angiomata present 
large spaces lined with endothelial cells (Fig. 46). Between these 




Fig. 46.— Cavernous angioma (Warren). 

spaces are parallel fibers of connective tissue which form the frame- 
work of the tumor. In cases involving the liver the proper sub- 
stance of this organ disappears completely, leaving only anastomos- 
ing spaces with a fibrous framework. Yirchow taught that the 
fibrous process was primary, and by traction and pressure gradually 
induced dilatation of the vessels and atrophy of the liver-substance. 
Some of the more recent writers believe that the dilatation of the 
vessels is the primary condition. The capsule sometimes found 
surrounding the cavernous angioma is certainly a secondary 
formation. 

Angiomata of the skin may enclose the hair-follicles and 
sweat-glands ) those of the subcutaneous tissue frequently show 
areas rich in fatty tissue (angiolipoma) ; secondary angiomatous 
change of tumors is probably the result of dilatation of the pre- 
existing or new-formed vessels. Sometimes secondary change 
may occur in the connective tissue of the vessels of an angioma, 
as in the plexiform angiosarcomata, in which the blood-vessels are 
surrounded by ensheathing sarcoma-cells (see Fig. 46). Certain 
cylindromata have the same origin. 



142 



TEXT-BOOK OF PATHOLOGY. 



Nature. — Angioma is essentially benign, and may continue 
through life without enlarging. Hemorrhage and innammatory 
or necrotic changes are its dangerous consequences. 

LYMPH ADENOMA. 

Definition. — This term is here used to designate a more or 
less malignant form of new-growth affecting the lymphatic glands 
or other lymphadenoid tissues, and having the structure of lym- 
phatic tissue. The lymphadenomata may be considered as forms 
of sarcoma, or at least as closely allieof to sarcoma. The term 
lymphosarcoma is sometimes applied, but is more appropriately 
given to growths of a more definite malignant nature, having 
the reticulated structure of lymphadenoid tissue. Other names 
applied to lymphadeuoma are malignant lymphoma and lymphoma. 

Etiology. — It is exceedingly difficult to establish the limita- 
tions of the term, and especially to decide whether or not certain 
cases in which definite etiologic factors have been discovered 
belong to the group under consideration or should be separated. 
There are cases of infectious enlargement of the glands and trau- 
matic swellings that cannot be distinguished histologically. In 
some cases even the clinical course is the same and a separation 
seems impossible. For example, the glands in a number of 
instances of Hodgkin's disease (as far as the clinician can es- 
tablish this diagnosis) have been found to contain tubercle-bacilli. 
We must conclude that general lymphatic tuberculosis may occur 
in the clinical form of Hodgkin's disease, but cannot assert that 
all cases of the latter are tuberculous. In other cases various 
micrococci and bacilli have been found, but none of these organ- 
isms have been shown to be specific. In a few instances bodies re- 
sembling protozoa have been discovered. 

Appearance and Seats. — Lymphadenomata present them- 
selves as more or less considerable enlargements of the lymphatic 
glands of a single group or more commonly of a number of groups 
in different parts of the body. All of the glands of the group 
may be involved, or only a few. The individual glands retain 
their shape, as there is usually no tendency to extension beyond 
•the capsule of the gland. In exceptional cases, however, the proc- 
ess is of a more infiltrating kind and the capsule is penetrated or 
destroyed. These instances merit the special term lympho- 
sarcoma. 

Lymphadenomata may be soft or hard, according to the amount 
of connective tissue and the denseness of the cellular infiltration 
and proliferation. On section the tumors are found to be grayish 
or whitish in appearance, and exceptionally may show slight areas 
of necrosis or softening. Extensive softening is exceedingly rare. 
The individual glands of the group may be clearly distinct, or may 



PROGRESSIVE TISSUE-CHANGES. 



143 



be fused together by interglandular connective-tissue overgrowth 
or by the penetration of the lymphadenomatous process through 
the capsule. 

When superficial lymphatic groups are involved tumors of 
various sizes are produced, and project as knobby or rounded en- 
largements beneath the skin. The latter is freely movable over the 
tumor unless the growth has penetrated the capsule or secondary 
inflammatory changes have occurred. In the case of internal 




Fig. 47— Lymphadenoma (lymphosarcoma) probably originating in remnant of thymus 
gland :'the tumor covered the upper part of the heart like a hood. The illustration 
shows the tumor turned upward and exposing the pericardium on its under surface. 

glands large intrathoracic or abdominal growths may be formed, 
and may exercise destructive compression of vital parts. 

Similar lymphadenomatous growths may spring from the lym- 
phatic tissues of the gastro-intestinal tract — tonsils, lymphatic 
follicles of gastric and intestinal mucosa. 

Sometimes the primary growth seems to begin in the thymus 
gland or its remnant (Fig. 47). Tumors of considerable size are 
produced in these cases, and their origin is recognized by their shape 
(Wo lateral parts united by a sort of isthmus) and hy the absence 
of the appearance of a conglomeration of glands. In these cases 
the adjacent glands, and later more distant groups, are involved. 
Lymphadenoma may be confined to the glands, but frequently 
extends to the solid organs by metastasis. The spleen, liver, and 
kidneys are the organs most frequently affected. They become 



144 



TEXT-BOOK OF PATHOLOGY. 



enlarged and indurated, and on section show light-colored areas of 
lymphadenoid tissue. Similar "lymphoid infiltration" may be 
seen in the heart, lungs, or other parts. 

Lymphadenoma may affect the bone-marrow secondarily and 
perhaps primarily. (Reference will be made to this under the title 
Myeloma.) Sometimes the tumors have a yellow or green color and 
are called chloromata (q. v.). 

Structure. — The finer structure of lymphadenomata is pre- 
cisely that of lymphadenoid tissues. There is a reticulum, more 
or less pronounced, formed by branching cells which are united by 
their prolonged extremities. In the meshes of this lie round cells 
containing large rounded nuclei. The cells are perhaps less 
uniform in size than those of normal lymphatic glands and large 
cells are more abundant. The secondary lymphomatous infiltra- 
tions of the spleen, liver, etc., have similar structure, but the 
reticulum is less distinct. Sometimes this may not be apparent in 
the primary growths ; in such instances the tumor is likely to be 
considered a simple round-celled sarcoma. 

Nature. — Lymphadenoma is variably malignant. In a small 
proportion of the cases this malignancy is of local character — that 
is, the growth tends to invade the neighboring parts. In most 
instances there is rather a tendency to general involvement of the 
lymphatic system, with metastatic deposits in various organs. To 
cases of this kind the terms Hodgkin's disease, pseudoleukemia, 
and adenia have been given. These cases present themselves in 
the form of a progressive anemia (lymphatic anemia — Wilks), often 
with irregularly relapsing fever (chronic relapsing fever — Epstein), 
and especially with lymphadenomatous tumors in the superficial or 
deep lymphatic groups (axillary, cervical, inguinal, mediastinal, or 
abdominal). The disease progresses more or less rapidly, and 
terminates in death from cachexia and exhaustion in from one to 
three years. Occasionally the course is rapid, repeated hemor- 
rhages or purpura may occur, and a fatal termination is reached in 
a few weeks or months. The whole course of the disease is sug- 
gestive of an infectious process. 

The relation of cases like the above and leukemia is certainly 
very close. The glandular tumors and the secondary changes in 
the organs are the same, excepting that the lymphatic glands are 
more prominently involved in ordinary lymphadenoma. The only 
striking difference is found in the blood. In leukemia there is 
marked and characteristic leukocytosis ; in the other condition this 
is absent. Many cases have, however, been observed in which 
Hodgkin's disease has become leukemia ; and some authors do not 
hesitate to speak of the two diseases as identical and representing 
merely two stages of a common affection. According to this view, 
Ave might classify cases as leukemic or aleukemic lymphadenoma. 
This view seems to me well grounded. 



PR GRESSIVE TISS UE-CHA NOES. 



145 



The blood in aleukemic cases shows more or less pronounced 
reduction in the number of red cells, and a normal, reduced, occa- 
sionally a moderately increased, proportion of leukocytes. The 
mononuclear leukocytes are sometimes in relative excess. In 
acute cases nucleated red cells may be found. 

The causes and nature of the irregular fever are uncertain. It 
may be due to an infectious cause, or may be the result of breaking 
up of leukocytes and liberation of ferments. 

Myeloma. — Certain cases present a hyperplastic condition of the bone- 
marrow that is comparable to lymphomatous affections of the glands. 
These may be instances of leukemia or thev may be non-leukemic. The 
process is sometimes diffuse and involves the marrow of a number of bones ; 
in other cases it is localized and tends to grow outward, destroying the 
bone and proliferating externally. The latter constitute myelosarcomata. 

SARCOMA. 

Definition. — The term sarcoma is applied to tumors composed 
of connective-tissue cells with very little intercellular substance. 
It is often said that sarcoma-cells resemble those of embryonal 
connective tissue ; more properly speaking, they may be likened 
to the ordinary connective-tissue cell falling short of complete 
development. There is little tendency in sarcoma to the forma- 
tion of fibrous intercellular substance, but a great tendency to 
continuous cell-proliferation. 

Etiology. — Of all the tumors sarcoma furnishes the best 
ground for Colmheim's theory. Its frequent occurrence in young 
persons, the relation of melanosarcomata to congenital pigment- 
spots of the skin, and the sarcomatous mixed tumors of the parotid 
and testis were cited by Cohnheim among the evidences pointing 
to a congenital origin. Traumatism and inflammation certainly 
play some part, either in stimulating sudden growth of a latent 
sarcoma or in developing a lesion from which sarcoma springs. 
The parasitic theory has gained many adherents in recent years. 
The resemblance to tubercle is very striking in certain cases and 
the peculiar dissemination is most suggestive. No specific form of 
bacteria, however, has been demonstrated, and experiments at im- 
plantation of the disease in animals have been unsatisfactory (von 
Eiselberg, Duplay and Cazin). Recently intracellular protozoan 
organisms have been described, but whether these are really organ- 
isms or cellular degenerations is doubtful. In some cases the 
structures described are certainly nuclear degenerations. It is 
not improbable that lymphosarcomata are due to the action of 
bacteria. 

In connection with the supposed infectious nature of sarcoma it is of 
interest to note that a relationship has been observed between syphilis and 
sarcoma. This is based on the fact that some cases disappear under anti- 
syphilitic treatment. 
10 



146 



TEXT-BOOK OF PATHOLOGY. 



Appearances. — Sarcomata are generally more or less rounded 
tumors often enclosed by capsule ; they may, however, be irregu- 
lar, infiltrating, and therefore unencapsulated. Some forms appear 
on surfaces, spreading as flat elevations more or less irregular in out- 
line. The consistency is soft or hard according to the number of 
cells and the amount of intercellular substance, or according to 
the kind and amount of associated tissue (myxomatous, chondrom- 
atous). Typical sarcoma, as the name implies (edpg, flesh), is flesh- 
like in consistency, and frequently on section the color is pink or 
of a flesh-tint. Many of the sarcomata, however, are quite white 
or gray, and a whitish liquid exudes from the surface on section. 

Dilatation of the blood-vessels may cause a decidedly hemor- 
rhagic appearance, and actual hemorrhages may take place, causing 




Fig. 48.— Secondary sarcomata of the lung: the primary growth was attached to the 

pleura. 

blood-cysts or, subsequently, serous cysts. Other degenerative 
changes, such as necrosis, mucoid change, and simple liquefaction- 
necrosis, may render sarcomata soft and often cystic. Sarcomata of 
glandular organs like the breast may present a cystic appearance 
in consequence of compression of the glandular ducts and acini 
and subsequent dilatation. 

Angiosarcomata (the variety in which sarcoma-cells spring 



PROGRESSIVE TISSUE-CHANGES. 



147 



from the adventitia of blood-vessels) present themselves as more 
or less irregular growths, frequently flattened and branching when 
the surfaces of organs are involved. 

Secondary sarcomata are nodular in character and nearly al- 
ways present a capsule if the size is at all considerable (Fig. 48). 
They are usually white or pinkish ; rather firm on section, but 
with a tendency to central necrosis or softening. In some cases 
almost every part of the body may be studded with minute white 
spots scarcely distinguishable from miliary tubercles. This con- 
dition is called sarcomatosis. 

Seats. — Sarcomata spring from pre-existing connective tis- 
sues, such as the subcutaneous, intermuscular, periosteal, or tendi- 
nous tissues ; bone, cartilage, fat, lymphatic glands, the submucous 
and serous surfaces. They may arise in the internal organs : kid- 
ney, liver, spleen, thyroid gland, testis. The individual seats will 
be further considered under the different forms. 

Structure. — The sarcoma-cell is rounded, cylindrical, spindle- 
shaped, or of polymorphous forms, the latter usually being larger 
than the round >r spindle-forms. The large number of cells in 
comparison with the amount of intercellular substance is always 
conspicuous. The cells themselves contain rather large nuclei of 
a somewhat vesicular appearance, though sometimes quite granular. 
In rapidly growing tumors karyokinetic figures may be very 
abundant ; less frequently the cells show evidence of direct divis- 
ion of the nuclei. Nuclear degenerations (karyorhexis, karyo- 
lysis, and hyperchromatosis) are frequent, and doubtless cause 
some of the appearances supposed to be protozoa. The arrange- 
ment of the cells in sarcomata is usually very irregular ; in some 
cases, however, particularly in spindle-celled sarcomata, the cells 
lie in fasciculi or parallel columns. The intercellular substance 
consists of a homogeneous matrix with a few fibers in the case 
of the spindle-celled variety, but with none at all in most other 
cases. The cells may be all of one type, but more frequently 
different forms or shapes occur in the same tumor. Among the 
polymorphous forms of cells may be noted large flattened cells 
resembling endothelial plates and giant-cells resembling myelo- 
plaques. (These forms will be discussed under the headings 
Endothelioma and Giant-celled Sarcoma.) 

The blood-vessels of sarcoma are usually channels lined with a 
single endothelial coat (see Fig. 50), but there may be more fully 
developed vessels. In some cases the vascular network is very 
conspicuous and forms the skeleton of the tumor, the sarcoma- 
cells being ranged round the vessels in the form of mantles and 
probably springing from the adventitia. Secondary changes may 
occur in the cellular masses surrounding the vessels, and peculiar 
forms of tumors thus result (see Cylindroma). 

Combinations of sarcoma with other forms of tumors are not 



148 



TEXT-BOOK OF PATHOLOGY. 



rare. All grades between the true sarcoma and the fibroma may 
be met with, and it is difficult to draw a line of distinction. 
Wherever a tendency to cellular proliferation is conspicuous and 
the formation of fibroblastic cells with elongated fibrous projec- 
tions is not conspicuous it is warranted to record the tumor as 
sarcomatous. Primary fibromata may become sarcomatous, and 
sarcomatous tumors perhaps at times become more benign by 
fibromatous transformation. Combinations with chondroma, os- 
teoma, myxoma, and other connective-tissue tumors; with adenoma, 
rhabdomyoma, and fibromyoma are not infrequent. More rarely 
the fibrous tissue of the benign tumors may undergo sarcomatous 
change. 

The structure of individual forms of sarcoma will be separately 
considered. 

Nature. — Sarcoma is essentially malignant. It tends to recur 
after removal ; it affects the general health of the patient ; and 
metastasis is frequent. Metastasis occurs through the circulation. 
The degree of malignancy varies greatly. The small round- 
celled and melanotic varieties are the most dangerous. Some 
forms, as the giant-celled and the fibrosarcomata, are compara- 
tively benign. The relatively benign form of tumor called recur- 
rent fibroid tumor by Paget is in reality a fibrosarcoma. The 
growth of sarcomata is usually rather rapid, and may become very 
rapid in consequence of irritation. 

Sarcomata are injurious to the general health 'in some obscure 
way. Jhe evidence of this is the anemia and leukocytosis and the 
irregular fever observed in various cases. The anemia may be 
trivial or severe, and may become extreme. Leukocytosis is fre- 
quent, but rarely marked. The polymorphous elements may be 
specially increased, but I have found the lymphocytes excessive in 
a number of cases. Irregular fever is often noted in lymphosar- 
coma and general sarcomatosis. Necrotic change may increase 
the tendency to fever. The exact influence of sarcoma on metab- 
olism is unknown. 

Spindle=celled Sarcoma. 

This form may consist of either large or small spindle-shaped 
cells with attenuated and sometimes branching extremities (Tig. 
49). Angular or stellate cells are not infrequent. The cells 
may be ranged in parallel columns, so that the tissue becomes 
quite compact ; and fasciculi of such cell-masses may run in differ- 
ent directions, interlacing, and thus giving the section a fibrous 
appearance. In other cases the cells present no definite arrange- 
ment. Spindle-celled sarcomata are harder than the round-celled 
varieties and usually more grayish or flesh-colored. They may be 
quite soft and white or degenerated and cystic. 



PROGR ESXIVE TISS UE-CHA NGES. 



149 



The amount of intercellular substance in some cases is quite con- 
siderable, and the term fibrosarcoma may be justified. It is very 




Fig. 49.— Cells from a large spindle-celled sarcoma (Ziegler). 



difficult sometimes to decide whether the tumor is sarcomatous or 
purely fibromatous. 

Spindle-celled sarcomata occur in the dense connective tissue 
of the periosteum, tendons, and fascia? ; less frequently in the 
softer tissues. They are relatively benign, some cases showing no 
tendency to metastasis, though recurring after removal. 



Round=celled Sarcoma. 

Sarcomata may be composed almost entirely of spherical or 
round cells, small or large in size. The designations small and 
large round-celled sarcomata are used, but do not really define 
separate varieties. The round cells when small resemble those of 





Fig. 50— Small round-celled sarcoma : in the center is seen a blood-vessel with its wall 

of endothelium. 



lymphatic organs. There is little intercellular substance. The 
blood-vessels may be quite large and hemorrhages with secondary 
changes may occur (Fig. 50). The larger cells contain relatively 
more protoplasm, frequently several nuclei, and not rarely different 
forms of cells (spindle-shaped and polymorphous) are associated. 

The naked-eye appearances of round-celled sarcomata are usu- 
ally quite characteristic. They are milky-white, gray, or pink in 



150 



TEXT-BOOK OF PATHOLOGY. 



color ; sometimes quite soft or cheesy in the center, and a milky 
liquid exudes. Cystic changes and even calcification may occur 
in the center. The small-celled variety is, as a rule, softer than 
the larger, though both are soft. 

Round-celled sarcomata are always malignant, the small-celled 
form being perhaps the most malignant of all varieties. 

lymphosarcoma is a variety of round-celled sarcoma. The 
appearance is the same as that of the other forms, but micro- 
scopically a close resemblance of structure with that seen in lym- 
phatic glands is discovered. The principal characteristic is the 
reticulum or stroma formed by branching stellate cells united by 
their prolongations. In the meshes of this reticulum lie lymphoid 
round cells (Fig. 51). The stroma may not be plainly visible 




Fig. 51.— Lymphosarcoma of nasal mucous membrane : a, on left side a blood-vessel, on 
right side reticulum; b, cells of reticulum; c, sarcoma-cells (Ziegler). 

unless sections are shaken to dislodge the cells from the reticulum. 
Lymphosarcomata occur in the lymphatic glands and lymphad- 
enoid tissues of the mucous membranes. Occasionally the thymus 
gland and other organs may be the seat. The distinctions from 
lymphadenoma have been discussed under that heading. 

Alveolar sarcoma is a sub-variety of round-celled sarcoma, 
though there are always spindle-cells as well. It is distinguished 
by the occurrence of acini filled with large round cells having a 
more or less decided epithelioid appearance. The stroma forming 
the acini is composed largely of spindle-shaped cells with a certain 
amount of fibrous tissue (Fig. 52). The blood-vessels supplying 
the tumors traverse these trabecule. The round cells within the 
alveoli may vary greatly in size, though they are usually large. 
The macroscopic appearance is not specially distinctive ; many 
of the cases, . however, are pigmented (see below). Alveolar 
sarcoma is most frequent in the skin, where it springs from moles 
and warts. It may also occur in the lymphatic glands, the serous 
membranes, and other parts. 

In some cases the alveolar appearance of the sarcoma is due to 



PROGRESSIVE TISSUE-CHANGES. 



151 



the fact that the sarcomatous proliferation has occurred in the 
adventitia of blood-vessels forming a plexus. In this way the 




Fig. 52— Alveolar sarcoma (Warren). 



meshes of the vascular plexus become filled with round cells 
and the alveolar appearance results. In other cases the alveolar 
character is due to the occurrence of sarcomatous foci of circum- 
scribed character in a connective tissue. These in their growth 
push the connective-tissue elements aside and thus form alveolar 
structures. 

Angiosarcoma. 

In this variety the sarcomatous proliferation begins in the ad- 
ventitious coat of blood-vessels (perithelioma). Certain authors 
have attempted to show that all forms of sarcoma originate in the 
blood-vessels ; this view, however, cannot be supported. Angiosar- 
comata are met with in the serous membranes, in the skin, and espe- 
cially in the salivary glands. Very rarely they occur in other parts 
of the body. The tumor is, as a rule, quite vascular, but may not be 
strikingly so. Sometimes telangiectatic change in the blood- 
vessels has been noted. Histologically these growths are charac- 
terized by round-celled masses surrounding the blood-vessels. 
The origin of the cells from the adventitia may be evident or ob- 
scure. In cases in which a vascular network is involved and 
each vessel has a coating of sarcoma-cells a plexiform appear- 
ance or arrangement results (Plexiform Angiosarcoma). In other 
instances in which a network of vessels is involved the sar- 
coma-cells accumulate in the vascular meshes in the form of cell- 
nests, and thus give rise to an alveolar form (Alveolar Angiosar- 
coma). Such forms occur in sarcomata springing from moles or 
warts. They are prone to melanotic change. The endothelium 



152 



TEXT-BOOK OF PATHOLOGY. 



of the vessels is occasionally the point of origin of vascular sarco- 
mata ; this form is a rare variety of endothelioma. The angiosar- 
comata are liable to degenerations, chiefly myxomatous (Fig. 53) 




Fig. 53.— Angiosarcoma with myxomatous degeneration (cylindroma) : the figure rep- 
resents one of the blood-vessels with the sarcomatous cells springing from its walls, and 
outside of these myxomatous tissue. 

and hyaline, and thus a certain proportion of the cases of cylin- 
droma (see below) have their origin. The blood-vessels may give 
way and hemorrhagic infiltration results. 

Angiosarcomata are in a measure benign, metastasis being very 
rare in the ordinary forms. The alveolar and melanotic varieties 
are highly malignant. 

Cylindroma. 

This term was originally applied by Billroth to tumors show- 
ing gelatinous masses or trabecular traversing their substance. 
Histologically different forms of growths may be distinguished. 
We deal here only with Sarcomatous Cylindromata. 

The latter may be simply sarcomata in which hyaline or 
myxomatous degeneration has occurred in more or less insular 
fashion, or in which sarcoma and myxoma are peculiarly com- 
bined. Nearly always there is some hyaline change with the myx- 
omatous. In most cases it is the angiosarcomata that present this 
peculiar condition. The sarcoma-cells surrounding the blood- 
vessels become converted into hyalomyxomatous tissue or cause 
the formation of this. There result branching columns of hyalo- 



PROGRESSIVE TISSUE-CHANGES. 



153 



myxomatous character traversing the sarcoma. In some cases the 
walls of the blood-vessels themselves may be the seat of hyaline 
change (Fig. 54), the proliferated sarcoma-cells surrounding the 





Fig. 54— Cylindroma showing pronounced hyaline degeneration of the walls of the 

blood-vessels. 



vessel being merely pushed aside. The term Angiosarcoma Myx- 
omatodes is given to these vascular forms. Cylindromata occur in 
the salivary glands, the brain, the lachrymal glands, and rarely in 
the subcutaneous tissues. In nature they are more or less benign. 



Melanosarcoma. 

Melanosarcoma, or pigmented sarcoma, is a form in which the 
tumor is dark colored from the presence of black or brown pig- 
ment. The latter, according to the careful chemical studies of 
Berdez and Nencki, contains no iron, and is therefore not simply 
blood-pigment. Ferruginous pigment has been found by certain 
authors, but is always outside the cells, and very probably is 
accidental, resulting from hemorrhagic extravasations. True mel- 
anotic pigment occurs in the cells or intercellular substance as 
a brownish-black granular matter, or in the cells as a diffuse stain. 
The tumor itself has not any definite characteristics aside from the 
pigment ; it may be round-celled (Fig. 55) or spindle-celled ; very 
frequently it is angiosarcomatous and alveolar in type. Melanotic 
sarcomata most frequently arise primarily in the skin, particu- 
larly in pigmented moles or warts, in the eye, or in the pia mater. 



154 



TEXT-BOOK OF PATHOLOGY. 



They are exceedingly malignant, often grow with great rapidity, 
and give rise to widespread metastasis, the liver being peculiarly 



, gpip ^ l 

Fig. 55.— Melanosarcoma, mainly round-celled : from a nodule in the skin. 

liable to involvement. The secondary growths have the same 
structure as the primary, and frequently are even more pigmented 
than the original tumor. 

Giant=ceIIed Sarcoma. 

This variety is characterized by the presence of large multi- 
nuclear cells resembling exactly the myeloplaques of bone. The 
remaining portions of the tumor may be spindle-celled or round- 
celled ; perhaps more frequently round and spindle-cells are asso- 
ciated. The giant-cells are often exceedingly large and contain 
several or many nuclei in the center of the cell (Fig. 56). The 
formation of these cells is most likely due to rapid nuclear multi- 
plication. In some cases they would seem to be caused by obliter- 
ation and transformation of capillary blood-vessels ; but the theory 
that they result from a fusion of cells seems unwarranted. Ziegler 
maintains that the presence of giant-cells does not form an essen- 
tial characteristic of a peculiar type of tumor, but that it is acci- 
dental, resulting from continued irritation. The occurrence of 
giant -cells in sarcomata of bones would then be explained by the 
constant irritation of the bony particles, while in other cases the 
presence of masses of blood-pigment in the sarcoma accounts for 
the development of giant-cells in the vicinity. This view is sup- 
ported by considerable authority and seems reasonable. 

Giant-celled sarcomata occur most frequently about bone, and 
the terms osteosarcoma and myeloid sarcoma have been given in 
consequence. They may, however, occur in other situations. 
Their nature is usually benign, metastasis being rare. 





Fig. 56.— Giant-celled sarcoma (Warren). 



The giant-celled sarcoma of bone is usually rather slow in 
growth, and gives rise to hard and irregular tumors, firmly attached 

_ — , 




Fig. 57.— Myelogenous osteosarcoma of the tibia (modified from Kast and Rumpel). 



to the bone-structures. It may begin within the bone as a myelog- 
enous form (Fig. 57) or from the periosteum. Secondary myxoma- 



156 TEXT-BOOK OF PATHOLOGY. 

tous or other change may cause more or less softening. The bone 
most frequently involved is the maxilla, the tumor known as epulis 
(sarcoma springing from the gums or alveolar processes) being 
generally a giant-celled sarcoma. 

MIXED TUMORS. 

All forms of connective-tissue tumors may be associated one with another; 
association of several forms are known as mixed tumors. Very frequently 
there is more or less sarcomatous tissue in such growths. With this will be 
found myxomatous, fibromatous, chondromatous, or osteomatous elements. 
The various constituents of the tumor are arranged with no special order, but 
simply present themselves as masses of cells or intercellular substance of 
different forms combined to make a heterogeneous tissue. Among the fre- 
quent seats of such mixed tumors the parotid gland and the testicle are 
most important. 

Chloroma. 

This tumor is no special form of new growth, but rather a variety of 
lymphosarcoma or round-celled sarcoma occurring with special frequency 
in the periosteum or the bones of the head and secondarily in other parts 
of the body. The name is applied because of the peculiar greenish pig- 
mentation of the cells. The nature of this pigment is not certainly deter- 
mined. Clinically cases of chloroma may present symptoms of leukemia 
or pseudoleukemia. 

Psammoma. 

This represents no distinct species of tumor-growth, but rather a pecu- 
liarity of different kinds. The name refers to the presence of calcareous 
matter like that of the brain-sand (acervulus cerebri), and psammoma has 
sometimes been called acervuloma. The calcareous matter occurs in the 
form of rounded masses or concentrically arranged whorls. The tumor- 
elements themselves may be fibromatous, gliomatous, sarcomatous, or even 
adenomatous or carcinomatous. In most instances it is angiofibromata or 
angiosarcomata that present these appearances. Psammomata are met 
with in the membranes of the brain, the choroid plexus, and the pineal 
gland. 

MYCOSIS FUNGOIDES. 

Mycosis fungoides or granuloma fungoides is a pathologic condition of 
the skin and subdermal structures having certain resemblances to sarcoma 
and to some of the infectious inflammations. 

Etiology. — Very little is known regarding the causes of this disease. 
Various bacteria, principally micrococci, have been discovered in the 
lesions, but none of these has been shown to be pathogenic. A few ob- 
servers have found bodies resembling protozoa ; but it is not certain that 
these were really animal organisms. 

Appearance. — The disease frequently presents distinct stages. First, 
the skin becomes somewhat swollen and red and presents eczematous 
lesions. In some cases the appearance is that of an erysipelatous inflam- 
mation. In the next stage nodular elevations occur, and finally tumors of 
considerable size, sometimes as large as an orange, and more or less fungoid 
in appearance. Necrosis is frequent and watery or bloody liquid is dis- 
charged. The tumors may have an angry, red appearance and have been 
likened to tomatoes. Kapid disappearance and reappearance of the tumors 
are a peculiar feature. 



PROGRESSIVE TISSUE-CHANGES. 



157 



Any part of the body may be affected and usually the lesions are mul- 
tiple. 

Structure. — Microscopically the structure of the tumors is allied to that 
of lymphadenomata. There is a proliferation of connective-tissue cells 
about the blood-vessels and glands at the base of the papillae of the skin, 
forming a network or reticulum in which round (lymphoid) cells are em- 
bedded. Epithelioid cells and giant-cells may occur. The tumors are 
poorly supplied with blood-vessels, and to this is attributed the tendency to 
central necrosis. Inflammatory infiltration (polymorphous leukocytes) is 
not observed to any considerable degree, excepting in the latter stages 
around and in the areas of necrosis. Mast-cells are often abundant. 

Associated Conditions. — In some cases, enlargement of the lymphatic 
glands, liver, and spleen has been observed, and has suggested the term 
pseudoleukemia cutis. Occasionally the blood presents leukemic char- 
acters. 

Nature. — The disease presents many resemblances to sarcoma or lymph- 
adenoma, and it has frequently been described as multiple sarcoma of the 
skin. In other respects it is allied to the infectious inflammations, though 
there is much less evidence of true inflammatory infiltration than in these. 
The relationship to leukemia and pseudoleukemia is unsettled. 

ENDOTHELIOMA. 

This tumor, which is also sometimes designated endothelial 
cancer, resembles cancer very closely in histologic appearances in 




158 



TEXT-BOOK OF PATHOLOGY. 



some cases. It appears, however, to be purely endothelial in 
origin, and therefore rather of the connective-tissue group or sar- 
comata. It affects the pleura, peritoneum, and membranes of the 
brain most frequently, but may be found in the skin, walls of the 
blood-vessels, periosteum, bone-marrow, lymphatic glands, and 
elsewhere. The serous membranes when affected become greatly 
thickened, tough, and white in color (Fig. 58), and irregular ele- 
vations or nodules may occur. Metastasis is infrequent, but the t 
adjacent organs are sometimes involved, and occasionally more 
distant structures. 




Fig. 59.— Microscopic section from the above (Fig. 58). 

Histologically the tumor is characterized by more or less 
tubular or acinus-like aggregations of endothelial cells. The 
latter vary in character from those which are distinctly endo- 
thelial to the most differentiated, which may be almost typical 
cylindrical epithelium (Fig. 59). Between these cellular columns 
or acini the connective tissue of the part affected may be seen in a 
normal state, though it is more frequently thickened by prolifera- 
tion. In the endotheliomata of serous membranes inspection of 
the sections shows that the columns of epithelioid cells occupy 
lymph-channels, and it may be possible to demonstrate that the 
endothelium of the latter has been the starting-point of the cel- 
lular proliferation. In cases of carcinoma with penetration into 
the lymphatic channels it is notable, on the other hand, that the 
endothelial lining of the channels is uninvolved. 

GLIOMA. 

Definition. — The term glioma is applied to tumors composed 
of neuroglia. It is difficult to distinguish between the circum- 



PROGRESSIVE TISSUE-CHANGES. 



159 



scribed tumors of this structure and the diffuse neurogliar hyper- 
plasia or gliomatosis is met with in certain cases. (See section 
on Diseases of the Nervous System.) ■ 

Etiology. — It is probable that congenital defects of develop- 
ment play some part in the causation of these tumors, particularly 
in the forms more frequently spoken of as gliosis. 

Appearance. — A typical glioma is usually a solitary tumor, 
rounded in outline, though its limits are difficult to determine, as 
it merges gradually into the surrounding nervous tissue. Gliomata 
are somewhat harder than the normal brain-substance, and often 
the color is a little different, either more grayish or pink or red- 
dish. Sometimes they are quite vascular and dark red. The 
normal shape of the part may be a little disturbed, or there may 
be indefinite elevation. In size the tumor varies up to masses as 




Fig. 60— Glioma of the corpora quadrigemina (Perls). 

large as a lemon. Diffuse gliomatosis causes a swelling of the 
affected parts, sometimes quite regular, at other times irregu- 
lar. When the spinal cord is affected its thickness may be con- 
siderably increased, On section the area of gliomatosis is rather 
firm and grayish in color. Nearly always there is a tendency to 
excavation or cyst-formation. In the cord this leads to the de- 
velopment of considerable cavities, as a rule communicating with 
the central canal. 

Seats. — Gliomata occur in the brain and less frequently in 
the spinal cord. In rare cases the cranial nerves have been in- 
volved. Glioma of the eyeball will be referred to below. Dif- 
fuse gliomatosis is particularly common in the cord. It is usually 
met with in the vicinity of the cavities of the brain or cord. 

Structure. — A glioma consists of cells containing rounded or 
oval nuclei with very little protoplasm and fine protoplasmic 
extensions which interlace and form an intercellular reticulum, 
giving the sections a granular appearance when viewed with low 
powers of the microscope. Special staining and higher powers 
may demonstrate the filamentous prolongations of the cells (Fig. 
60). The number of cells and the density of the intercellular 
network vary greatly. As a rule, the cells are larger than the 
normal neuroglia-cells, and sometimes they contain several nuclei. 



160 



TEXT- BO OK OF PATHOLOGY. 



The tumor is generally quite vascular, and occasionally telangiec- 
tatic vessels may be observed. Secondary hemorrhages are prone 
to occur in the latter case. Softening may occur, and occasionally 
sarcomatous transformation has been described, though with 
doubtful propriety. 

Diffuse gliomatosis has similar microscopic appearances, though 
the tissue is likely to be more compact and less vascular. In the 
spinal cord the process begins as a subepithelial proliferation of 
the glia at the posterior raphe of the central canal, the lining 
epithelium of this at the same time undergoing a certain amount 
of proliferation. Subsequently the gliomatosis increases and cavities 
form within. These may be lined with epithelial or epithelioid cells 
which are occasionally ciliated. Gliomatosis may also present 
itself in the form of scattered nodular hyperplasias of the neuroglia. 

Nature. — Glioma is essentially benign. It is dangerous 
mainly on account of the pressure it exerts. Sarcomatous trans- 
formation may possibly occur. The growth of the tumor is rather 
slow. 

Glioma of the eyeball is a form of tumor that is sometimes considered 
true glioma. It is, strictly speaking, a round-celled sarcoma. It springs 
from the retina and resembles in structure the granular layer of the retina. 
It occurs most frequently in children, particularly in early life (two to four 
years), and often on both sides simultaneously. Family predisposition, in 
some cases, is very striking. Extension along the optic nerve or externally, 
and a tendency to recurrence after removal, indicate the malignant char- 
acter of the growth. 

Glioma Ganglionare. 

Definition. — This term indicates a form of mixed tumor composed of 
neuroglia and nerve-fibers with large ganglionar nerve-cells. 

Etiology. — Probably congenital abnormality of development furnishes 
the groundwork for the subsequent development of these tumors. 

Appearance. — A ganglionar glioma may resemble the ordinary glioma, 
occurring as a solitary tumor, the outlines of which are difficult to dis- 
tinguish from the surrounding tissue. More frequently it occurs in the 
form of multiple nodular condensations scattered through the brain or 
cord. The contour of the affected parts may not be altered, and on section 
the growths may be recognized only by the light-colored patches and areas 
of increased density. A few cases of ganglionar gliomata of the spinal or 
sympathetic ganglia have been described. In these cases the tumors ap- 
pear as rounded enlargements of the affected ganglia. Occasionally the 
nerve-roots are seats of these tumors ; the suprarenal capsules may also 
be affected. 

Structure. — The definition indicates the usual structure. The glia- 
fibrils are generally conspicuous in number, the nuclei being comparatively 
few. Traversing the tumor there may be more or less abundant nerve- 
fibers with or without medullary sheaths. Large ganglionar cells may be 
found in considerable abundance or in small number. The vascularity of 
the growths differs greatly. 

Nature. — The nature of these tumors is the same as that of the ordi- 
nary glioma. 



PROGRESSIVE TISSUE-CHANGES 



161 



NEUROMA. 

Definition. — Strictly speaking, neuroma is the term applied 
to tumors composed of nerve-fibers. Ordinarily, however, the 
name is iriven to fibrous growths springing from the perineurium or 
endoneurium of nerves. The terms true and false neuroma dis- 
tinguish between the two forms. True neuromata are exceed- 
ingly rare. 

Etiology. — Very little is known regarding the causation. 
Injury may play a part, as in the case of amputation-neuromata. 

Appearance. — False neuromata occur as nodular thickenings 
along the course of nerves. They may be fusiform or elongated, 
may extend considerable distances along the nerves, and may 
form networks of ridges or elevations when the peripheral nerves 
are involved (Plexiform Neuroma). As a rule they are multiple, 
and sometimes occur in exceedingly great numbers scattered over 
the entire body or involving a single part of the body, as the 
nerves of the arm or leg. After amputations rounded thickenings 
may occur at the ends of the nerves and cau^e painful conditions 
of the stump. 

Seats. — The peripheral nerves are most frequently involved, 
but the nerves may be implicated near their roots, or the terminal 
fibers within the organs may become affected. 

Structure. — Ordinary false neuroma consists of fibrous tissue 
in the form of reticular connective tissue with greater or less 
abundance of cells pushing aside or surrounding the nerve-fibers 
proper. The latter are prone to degenerate in consequence of the 
pressure. Proliferation of the nerve-fibers has sometimes been 
described, but it is doubtful whether such actually occurs. More 
probably the existing fibers increase in length and form a mass 
by curling at the end. True neuromata of two kinds are de- 
scribed : those composed of medullated and those consisting of 
non-medullated nerve-fibers. The former are called myelinic, the 
latter a myelinic. 

Nature. — Neuromata are painful tumors, but benign in a 
pathologic sense. Their growth up to a certain point is often 
rapid. 

LEIOMYOMA. 

Definition. — Leiomyoma, or myoma lsevicellulare, is a tumor 
containing smooth muscle-fibers. Nearly always there is a cer- 
tain amount of fibrous tissue associated, and in the most com- 
mon form, myomata of the uterus, there is always considerable 
fibrous tissue, and the term fibromyoma is appropriate. Occasion- 
ally a few unstriped muscle-cells may be seen in tumors of other 
kinds. 

Etiology. — Some of the myomata of the uterus exhibit 
glandular acini in the interior and suggest a congenital origin, 
11 



162 



TEXT-BOOK OF PATHOLOGY. 



This, however, is by no means certain. In other cases there are 
features suggesting that irritation is the important cause, though 
this also remains to be proved. 

Appearance. — Leiomyomata are usually rounded growths, 
varying in size from minute nodules to huge solid masses weighing 
as much as sixty to seventy pounds. The largest (heaviest) solid 
tumor I have ever seen was a degenerated fibromyoma weighing 
eighty pounds. Leiomyomata are surrounded by a capsule more or 
less well developed and are generally quite hard, though secondary 
degeneration at times alters the consistency, making the tumor quite 
soft in the case of mucous transformation, or stony-hard when cal- 
cification has occurred. On section through the growths the 
stratified or fasciculated arrangement of the cells is visible to the 
naked eye. Concentric layers may be apparent, or a more wavy 
irregularity may be seen. They are grayish or flesh-colored, or in 
rare instances quite red (myoma cavernosum) in consequence of en- 
larged vascular channels. Central softening may lead to cystic 
change (myoma cysticum). 

When the myomata spring from the submucous or subserous 
tissues they may become polypoid, hanging from a point of attach- 
ment by a narrow pedicle. In rare instances the latter is 
severed and the tumor becomes a free body. Submucous myo- 
mata of the uterus may thus eventually be discharged after a 
spurious labor. Subserous myomata may become free in the 
peritoneal cavity. 

Myomata of the uterus may have three situations — submucous, sub- 
serous, or interstitial. In the latter, the tumor occupies the wall of 
the uterus without any tendency to project particularly toward either sur- 
face. Uterine myomata are usually multiple, occur during the third and 
fourth decades of life, continuing their growth until the menopause and 
usually decreasing after that epoch. They endanger life by their pressure 
and by the copious uterine hemorrhages which they occasion. Very fre- 
quently salpingitis is associated, and recently attention has been called to 
degenerated conditions of the myocardium in patients suffering from uterine 
fibroids. 

Myomata of the skin occur in younger patients, even in childhood, and 
are generally multiple and often painful (tubercula dolorosa). 

Seats. — The common situations are the uterus, the gastro- 
intestinal tract, and the ovaries ; the less common seats are the 
walls of the blood-vessels, the skin, and the nipple. In all situa- 
tions the tumor springs from pre-existing unstriped muscle-fiber. 
In most cases, according to some authors, the origin is in the walls 
of the minute blood-vessels, but direct origin from the muscular 
layer of the affected organs, or from the erectores pilorum in the 
case of the skin, cannot be denied. Myomatous metaplasia of the 
connective tissue, as in the case of myomata originating in the 
areas of old pleural thickening, has been assumed, but is im- 
probable. 



PROGRESSIVE TISSUE-CHANGES. 



163 



Structure. — As has been said, association with fibrous tissue 
is usual. Microscopically the tumor presents* a characteristic 
appearance. Bundles of muscle-cells are seen running in different- 
directions. Those cut longitudinally show cylindrical nuclei as 
the most conspicuous feature, the outlines of the cell being indis- 
tinct (Fig. 61). Where the cells are transversely cut the nucleus 




Fig. 61.— Leiomyoma of uterus. 



presents a circular outline with clear protoplasm surrounding it. 
The picture of a leiomyoma is often suggestive of sarcoma, but 
may be distinguished by the greater regularity in direction of the 
cells in different bundles and by the more distinctly cylindrical out- 
line of the nucleus. The cells of leiomyomata may be isolated by 
maceration of the sections in 20 per cent, solution of nitric acid 
for twenty minutes, or in 30 per cent, solution of caustic potash for 
fifteen minutes. They are spindle-shaped structures containing a 
nucleus about one-third the length of the entire cell. 

Leiomyomata are generally poor in blood-vessels, but may 
show a teleangiectatic condition of the vessels. The lymphatic 
spaces may similarly dilate, forming cystic spaces containing 
spontaneously coagulable material. 

Of the degenerative changes calcification is the most common, 
particularly in the uterine fibromyomata. This begins in the 
center of the tumor, but may eventually involve the whole mass. 
Myxomatous change may occur in myomata containing much 
fibrous tissue, and sarcomatous transformation has been described, 
but is rare. 

Nature. — The nature is eminently benign. Myomata of the 
digestive tract may cause occlusion or strangulation, or by their 
weight may exercise serious traction. Uterine myomata are dan- 
gerous in the ways already indicated. The growth is usually 
slow. 



164 



TEXT-BOOK OF PATHOLOGY. 



RHABDOMYOMA. 

Definition. — Rhabdomyoma, or myoma striocellulare, is a tu- 
mor containing more or less striped muscle-fiber. Usually there 
is but a small quantity of the latter, the bulk of the tumor being 
of some other tissue, most frequently sarcomatous. 

Etiology. — Congenital defective development seems an im- 
portant cause, as the tumors occur in early life and in situations 
in which striped muscle-fiber does not normally occur. 

Appearance and Seats. — The rhabdomyomata of the kid- 
ney (the most frequent seat) present themselves as large rounded 
or irregular masses, more or less encapsulated. In the testicle 
they are similar, though of smaller size. A few cases have been 
described in which irregular tumors of the retroperitoneal tissues 
have contained muscle-fibers. 

Structure. — The microscopic appearance is usually that of a 
spindle-celled sarcoma, containing more or less striped muscle-fibers. 
These are elongated spindle-shaped cells, partly striated, and sug- 
gesting embryonal muscle-tissue and rarely more fully developed 
muscle-fibers. Large areas of the tumor may contain no muscle- 
fiber at all, while certain portions are richly supplied. Adenoma- 
tous elements are not rarely associated. The tumors of the kidney 
which contain striped muscle-fibers are in the main sarcomatous or 
adenosarcomatous. 

Nature. — These tumors are malignant in proportion as the 
sarcomatous element is predominant. Metastasis is, however, 
infrequent. General cachexia and hemorrhages reduce the vitality 
and lead to fatal termination. 

PAPILLOMA. 

Definition. — The term papilloma indicates a tumor arising 
from the surface and covered with epithelium representing more 
or less accurately the structure of the papillae of the skin. 

Etiology. — It is difficult to draw a line between certain papil- 
lomatous growths that are the result of chronic irritation and others 
that arise in a seemingly spontaneous manner. It would appear 
that irritation is an important factor in most, if not all, cases, but 
there is also no doubt some form of predisposition. Whether this 
resides in structural peculiarities or not is difficult to determine. 
A peculiar form of inflammatory growth resembling the sponta- 
neous papillomata is that known as venereal wart. It occurs about 
the genitalia or anus and especially after gonorrhea, Another 
form of inflammatory papillomata is that found in the mucous 
membranes surrounding carcinomata or chronic ulcerations of 
syphilitic or other kinds. 

Appearance. — The most familiar form of papilloma is that 
which occurs in the skin and which is commonly called wart 



PROGRESSIVE TISSUE-CHANGES. 



165 



Warts or papillomata may be single, but more frequently occur in 
groups, and there may be many growths in widely scattered areas 
of the body. A wart may be simply a 
smooth hemispherical elevation, or it may 
have a cauliflower appearance. The epi- 
dermis covering it is, as a rule, somewhat 
more granular or rough than is that of the 
normal skin. The size of these growths 
varies from minute points to nodules as 
large as a walnut. On the mucous surfaces, 
especially where the epithelial covering is 
columnar, the papilloma presents itself as 
a soft and more distinctly cauliflower 
growth (Fig. 62). It is red in color, or, 
if the epithelium is stratified and squamous, 
grayish or pink. The growth is usually 
comparatively hard when covered by 
squamous epithelium. 

Two varieties are sometimes distin- 
guished. The hard papillomata, such as 
those which occur in the skin, and the 
soft papillomata, or the form usually seen 
in the mucous membranes. 
Seats. — Papillomata occur in the skin of the neck, hands, 
back, and other parts, and in the mucous membranes, particularly 
in the bladder, larynx, nasal chambers, and gastro-intestinal tract. 
Small papillomatous outgrowths may spring from the lining mem- 
brane of glandular ducts, as in the breast or ovary. These may 
lead to subsequent cystic change in the organ, or they may arise 
after cystic change has begun by proliferation of the lining mem- 
brane of the cyst. 

Structure. — The essential parts of papilloma are the center 
or groundwork of connective tissue containing blood-vessels and 
the epithelial covering. In the skin the growth imitates the nor- 
mal papillae, all portions of the latter, however, being greatly 
exaggerated. When there is tendency to cauliflower appearance 
the papilloma shows a branching form on vertical section. Each 
of the branches contains a connective-tissue framework with an 
epithelial covering. The latter consists of stratified, squamous cells 
and shows a decided tendency to horny change. Distinct concen- 
tric whorls of horny epithelium, such as occur frequently in epi- 
theliomata of the skin, may be met with in papillomata. In some 
cases the amount of connective-tissue groundwork in the papilloma 
is excessive ; in others the new-growth consists almost entirely of 
proliferated epithelium. In some of these latter cases the resem- 
blance to epithelioma may be quite suggestive, but a distinction 
can be made by observing that the tumor tends to grow outward 




166 



TEXT-BOOK OF PATHOLOGY. 



rather than into the deeper structures, and always shows some 
connective-tissue stroma at least. The papillomata of the mucous 
membranes differ according to their situation. In the larynx and 
other portions covered with squamous epithelium they may present 
much the same appearance as that seen in the skin, though the 
epithelium, as a rule, remains softer. There are cases, however, 
in which a distinct pachydermatous change is found in the epi- 
thelial covering of papillomata. In the gastro-intestinal tract and 
in the bladder papillomata are prone to be soft and villous in 
appearance and are covered with a scantier epithelial coating. 
Cystic change is not unusual as a result of degenerative processes 
or of distention of the mucous glands. 

Nature. — The nature of these tumors is benign, but they may 
be destructive of the general health in consequence of repeated 
hemorrhages or by interfering with the function of the organ or 
part in which they are situated. In some cases they are supposed 
to become malignant, but this has not been definitely proved. 

ADENOMA. 

Definition. — Adenoma is the term applied to a new-growth 
corresponding more or less in structure with certain epithelial 
glands, and therefore presenting acini or tubules containing 
glandular epithelial cells (cylindrical or polyhedral) and a reticu- 
lum of connective tissue and blood-vessels. It is difficult to 
separate simple glandular hyperplasia on the one hand and carci- 
noma on the other hand from true adenoma. This will be dis- 
cussed in referring to the structure. 

Etiology. — The causation of adenoma is obscure. In some 
cases congenital misplacements of tissue-elements appear to play 
a part, as is seen in the cases of adenomata of the kidney having 
the structure of suprarenal bodies. These tumors which, it is true, 
some authorities refuse to consider as adenomata, have a general 
resemblance to adenomata and spring from remnants of suprarenal 
tissues embedded in the kidney-substance. Traumatism may be 
a factor in the etiology by exciting the proliferation of such mis- 
placed tissue-elements. In other cases the ordinary glandular 
structures seem to be stimulated to abnormal hyperplasia and 
tumor-growth in consequence of continued irritation. 

Appearance. — The appearances of adenomata vary greatly 
Avith their seat. On the mucous surfaces there may be a simple 
thickening or more or less diffuse and irregular elevation of the 
surface, or in other cases distinct papillomatous outgrowths and 
rarely definite nodular tumors. In some of these cases the condi- 
tion is purely one of inflammatory hyperplasia ; in other cases 
there is undoubted tumor-growth. No sharp demarcation can be 
established. In the substance of the organs adenomata occur as 



PROGRESSIVE TISSUE-CHANGES. 



167 



nodular tumors, usually singly and well circumscribed, and not 
rarely surrounded by a fibrous capsule. They are moderately 
firm, and on section whitish or pink in color. Sometimes cystic 
change occurs as the result of dilatation of the glandular acini or 
in consequence of degenerative softening ; in these cases the con- 
sistence is correspondingly altered. 

Seats. — Among the situations in which adenoma is frequent 
may be mentioned the mucous membranes, the skin, and certain 
organs, notably the mammary gland, liver, kidney, suprarenal 
bodies, thyroid gland, and ovaries. Clinically important seats are 
the pylorus, the duodenal papilla, the rectum, and the uterus. In 
these situations adenomata spring from the epithelial tubules or 
mucous glands. In the skin the points of origin are the sebaceous 
and sweat-glands. 

Structure. — The definition in general indicates the structure 
of these tumors. They are more or less typical ; that is to say, 
there are acini of normal appearance presenting a single layer of 
columnar epithelium, with perhaps in places a tendency to heaping 
up the several rows of epithelial cells. These acini are well in- 
closed by a surrounding connective-tissue reticulum, and the 
appearance of normal gland-tissue is thus produced. Unlike 
normal glands, there are no excretory ducts, or at most imper- 
fectly developed ducts. 

Two varieties of adenoma are sometimes distinguished, the 
tubular and the racemose or alveolar. In the former the glandu- 
lar system is simple and consists of tubular formations lined with 
columnar epithelial cells ; in the latter the appearance is that of 
more complicated glands with closely aggregated acini of circular 
outline containing columnar and often cubical or polyhedral cells. 
The number of varieties may be carried further, however, for in 
the liver the adenomata resemble the normal liver-structure rather 
than the ordinary glandular formation above described, while in 
the suprarenal capsules and kidney the appearance is that of 
slightly atypical suprarenal structure, or in other cases that of 
embryonal renal tubules. 

With the further growth of adenomata the appearance may be 
little changed. In other cases considerable variations occur, and 
there is a tendency, more marked in some situations than in 
others, to active proliferation of the epithelium, which may cause a 
considerable alteration in the appearance of the tumor, and event- 
ually transformation into definite carcinoma. In other cases the 
structure from the beginning is so atypical and the epithelial pro- 
liferation so irregularly active that the term adenocarcinoma is 
applicable. 

The connective-tissue stroma of adenomata may be moderate 
in quantity or may be considerable. In some adenomatous 
proliferations of the mucous membranes the number of gland- 



168 



TEXT-BOOK OF PATHOLOGY. 



acini or tubules may be relatively small, while the interglaudular 
connective tissue shows active round-cell infiltration to a very 
considerable degree. Sometimes the interglandular tissue is dis- 
tinctly sarcomatous (adenosarcoma). In other instances the bulk 
of the tumor may consist of connective tissue of fibrous character 
in which are embedded a relatively small number of glandular 
alveoli. In all of these cases it is difficult to determine whether 
the connective-tissue process was primary and the epithelial sec- 
ondary, or the reverse. 

Secondary changes are common, the adenomata of the stom- 
ach and uterus being particularly prone to change their char- 
acter to that of carcinoma. In these cases there may be noted 
active proliferation of the epithelial cells, so that the acini or 
alveoli become completely filled, or that the ends of the tubular 
structures become blocked up. There is a tendency to extension 
of epithelial infiltration beyond the limits of the acini, cancerous 
outgrowths being the result. In other cases the malignancy is 
manifested by the excessive epithelial proliferation in the form of 
new acini of irregular character (Fig. 63). This form is known 

s hy\ ^ - c „ v i \ * \ v ^» 



Fig. 63.— Destructive adenoma (Beyea). 

as destructive adenoma, adenoma destruens, or adenocarcinoma. 
Eventually the tumor may become purely carcinomatous ; in 
other cases, however, it continues to increase in size, always re- 
taining its adenocarcinomatous appearance, but never becoming 
typically carcinomatous. 

Degenerative changes may be met with as in other tumors. 
Hyaline transformation or production may give the tumor an 



PROGRESSIVE TISSUE-CHANGES. 



169 



appearance justifying the term '' cylindroma " or " cylindro-aden- 
oma." Such cases are rare. Myxomatous and even calcareous 
change may sometimes be observed. The connective-tissue stroma 
may proliferate actively and assume sarcomatous appearances — 
adenosarcoma. Cystic change may result from gradual dilata- 
tion of the glandular acini or from distention of normal ducts 
or alveoli of the gland in which the tumor occurs. In these cases 
the term cystic adenoma or cyst-adenoma is applicable (Fig. 64). 




Fig. 64.— Adenoma of the mammary gland, with cystic enlargement of acini and abundant 
interglandular hyperplasia of connective tissue. 

Nature. — Adenomata are benign tumors. In some cases, 
however, a pure adenoma may give rise to metastasis. Those of 
the liver, for example, not rarely cause secondary deposits in the 
spleen and less frequently elsewhere. The adenomata of the 
thyroid gland similarly cause metastasis, though it is less certain 
that these are to be considered as pure adenomata. Destructive 
adenomata or adenocarcinomata are malignant in proportion to 
the amount of carcinomatous transformation. 

The effect of adenomata on the general health is variable. 
They do not contribute to the organic metabolism as far as is 
known, though occasionally biliary pigmentation of the adenomata 
of the liver and the secretion of milk-like fluid in mammary 
adenomata evidence the partial preservation of function by the 
cells. The general health may be unfavorably influenced by 



170 



TEXT-BOOK OF PATHOLOGY. 



adenomata of the mucous surfaces in consequence of their inter- 
ference with normal functions or in consequence of secondary 
ulceration and hemorrhage. 

CARCINOMA. 

Definition. — The term carcinoma or cancer may be applied to 
tumors in which epithelial proliferations in the form of solid blocks 
or columns, or in the form of atypical acini, separated by more or less 
connective tissue, present themselves, the epithelial proliferation 
showing a tendency to extend beyond normal anatomic limits. 
It is extremely difficult to construct a definition that will be 
universally applicable. Some have regarded the tendency of the 
epithelial proliferation to break through the normal limits and 
extend beyond the confines of the epithelial structures from which 
it rises, as the important fundamental element of carcinoma. 
Others have held that there is a peculiar atypical character in the 
epithelial cells themselves, shown by irregular cell-division, hyper- 
chromatosis, and other features. The older authors believed that 
polymorphism and certain irregularities of cell-contour suffice to 
distinguish carcinoma-cells from normal cells or those of other 
tumors ; but this polymorphism is now recognized to be the result 
entirely of compression in the growth of the tumor, and to be 
therefore accidental. Some have believed that the term car- 
cinoma should include all epithelial tumors giving rise to metas- 
tasis, but this necessarily restricts the term too greatly on the one 
hand, and, on the other hand, includes certain tumors probably 
purely adenomatous. I prefer to regard as carcinoma any 
epithelial growth atypically reproducing certain glandular or 
other structures and showing a manifest tendency to irregular 
extension. 

etiology. — The causes and nature of carcinoma are still 
obscure. A number of theories have been offered. These may be 
considered under different headings. 

(a) Congenital Theory. — The theory of Cohnheim regarding the 
etiology of tumors in general is less applicable to cancer than to 
certain other growths. There are a few examples, however, which 
would seem to prove that misplaced epithelial cells undergo car- 
cinomatous proliferation ; for example, there are cases of appar- 
ently primary carcinoma springing from bones which would seem 
to require this explanation. It is not always certain, however, 
that such cases are actually primary. They may represent metas- 
tases from small primary growths which have escaped notice. 
The rarity of carcinomata in early life would seem to negative 
the congenital theory, and at all events would show that other 
influences of importance are requisite. Of late, a number of 
hypotheses that in a measure contain the idea of congenital 



PROGRESSIVE TISSUE-CHANGES. 



171 



origin have been put forward to explain the formation of car- 
cinoma. In these there are assumed some form of peculiar irregu- 
larity in cell-multiplication, and a tendency to independent pro- 
liferation supposed to originate in faulty development. These 
hypotheses are vague and uncertain. 

(6) Traumatic Theory. — Clinicians are inclined to give great 
weight to this. A single traumatism probably has little import- 
ance, though women frequently state that they recall distinct 
injuries from which carcinoma of the breast has seemed to 
originate. It must be recalled that such injuries are sustained by 
practically every woman, and the presence of carcinoma would 
readily be attributed to a preceding hurt. In cases of epithe- 
liomata of the lip in pipe-smokers, in the carcinomata of the 
scrotum and limbs in chimney-sweeps and paraffin-workers, 
and in cases of uterine carcinomata following laceration of 
the cervix, the effect of chronic irritation would seem to be 
important. 

(c) Parasitic Theory. — The peculiar growth of cancer, its de- 
structiveness of the general health, and its metastasis readily 
suggest an infective' origin. Bacteriologists sought to isolate 
micro-organisms without success ; later investigators have turned 
their attention to low forms of animal life, protozoa. (For further 
discussion, see Animal Parasites.) A few successful experiments 
have been made at implantation from man to animals, or from one 
animal to another ; but as Hanau, one of the few successful ex- 
perimenters in this work, himself states, these experiments do not 
prove infectiousness. The secondary growths in the second ani- 
mal may be simply of the nature of metastasis, due to implantation 
of the cancer-cells and subsequent proliferation. Occasionally an 
endemic occurrence of carcinoma has been claimed, and some au- 
thors have even referred to houses in which carcinoma frequently 
arose. 

(d) Tumor-dyscrasia. — This indefinite term is supposed to indi- 
cate a tendency to cancer-growth probably due to peculiarities of the 
liquids of the body. No proof of the existence of any definite 
dyscrasia has ever been furnished, though it is apparent on study 
that some form of disposition to this growth acts as the predis- 
posing cause, even if traumatism, infection, or other factors are 
the immediate cause. 

Age plays an important part in the formation of carcinoma, 
as this tumor is essentially one of adA T anced years. Among 275 
cases collected by Lubarsch, 55.6 per cent, occurred between the 
ages of forty-five and sixty-five. There were a few instances in 
childhood and early life. Between fourteen and nineteen there 
were 1.46 per cent. ; between twenty and twenty-five, 1.8 per 
cent. ; between twenty-six and twenty -nine, 1.1 per cent. The 
frequency in later life was formerly ascribed to some alteration in 



172 



TEXT-BOOK OF PATHOLOGY. 



the vitality of the epithelial cells, rendering them more liable to 
abnormal proliferation. The nature and cause of such alteration, 
however, remain obscure and theoretical, though there is certainly 
a greater tendency to cancer-growth as age increases. 

Heredity was formerly regarded as of great importance. Cer- 
tainly in some cases there seems to be hereditary transmission of 
the tendency to develop carcinoma. 

Appearance. — Carcinomata differ considerably in appearance 
in different parts of the body. Those of the surfaces present 
themselves as more or less nodular, flat elevations. In the skin 
the nodules may remain hard and rather smooth, or they may 
soften upon the surface, forming unsightly ulcerations. In the 
mucous membranes the growths are more frequently soft and poly- 
poid or cauliflower-excrescences (Fig. 65). Ulceration may occur 




Fig. 65.— Carcinoma of the duodenal papilla (modified from Kast and Rumpel). 

on the surface of such elevations, or from the first the tumor may 
be of ulcerative character, causing spreading excavations limited 
by thickened projecting edges. Carcinomata of the glandular 
organs form more or less nodular tumors or irregular infiltrations. 
These vary greatly in consistency, some being almost stony hard, 
others soft in consequence of their preponderating cellular char- 
acter or of secondary degenerations. On section the tumor is found 
to be white or grayish in color, generally somewhat translucent 
and glistening, and milky liquid may ooze from the surface. Cap- 
sule-formation is rarely seen, though in occasional instances the 
normal connective tissue of the organ is pressed outward by the 
growth of the tumor, and thus forms an imperfect capsule. The 
primary growth is nearly always solitary. Occasionally instances 
are observed in which two separate masses develop simultaneously 



PROGRESSIVE TISSUE-CHANGES. 



173 



and apparently independent of each other : as in the two breasts. 
More frequently apparent multiplicity is caused by the early ap- 
pearance and rapid growth of metastases. 

Secondary carcinomata are nodular in character and nearly 
always multiple. The larger are often distinctly encapsulated. 
Central softening or contraction of connective tissue may give the 
surface of the nodule an umbilicated character (Fig. 66). The 




Fig. 66.— Metastatic nodules of carcinoma on the surface of the liver (Hanot and Gilbert). 

number varies greatly, from a few large or small nodules to innu- 
merable tubercle-like forms in general carcinomatosis. In some 
situations, as in bones, secondary carcinoma has an infiltrating 
character. 

Seats. — The situations in which carcinomata occur are very 
numerous ; they invariably arise ' from pre-existing epithelial 
structures. In the rare instances in which a presumably primary 
carcinoma has occurred in bone or other connective tissues, the 
presumption is warranted that the tumor originated from remnants 
of epithelial tissue left by faulty development. Among the fre- 
quent places of origin the most important are the uterus, the skin, 
the gastro-intestinal tract, particularly the esophagus, pylorus, and 
rectum, the mammary gland, the ovaries ; less frequently the liver, 
kidney, thyroid gland, prostate, or testicle may be the starting- 
point. Secondary carcinomata curiously do not often affect parts 
in which the primary growth is frequent. Of the many seats 
of secondary carcinoma, the lymphatic glands, the liver, spleen, 
lungs, heart, and serous membranes are the most important. Sec- 
ondary carcinoma of the bones is specially frequent after carcinoma 
of the breast or the thyroid gland. 

Structure. — The histology of carcinoma varies greatly in dif- 
ferent situations and in different forms. There are two distinct 



174 TEXT-BOOK OF PATHOLOGY. 

elements involved — viz., epithelial cells and a connective-tissue 
stroma. The epithelial cells are medium-sized or large, and have 
a rather large and clear nucleus ; the shape of the cell, however, 
differs widely. In epitheliomata of the skin the cells are large and 
of a squamous variety. In carcinomata of mucous membranes they 
are more often cylindrical or columnar, and there is a tendency to the 
formation of cuboidal or polyhedral epithelium. The last-named 
forms are habitually present in the cancers of glandular organs. 
The mutual compression exercised may occasion a polymorphous 
character, and the older writers regarded this as a distinctive feature 
by which a carcinoma-cell could be recognized as such. Secondary 
changes may occasion wide variations in the appearance of the cells ; 
thus the epithelia of cancers of the skin tend to become arranged in 
concentric whorls and at the same time to become somewhat 
glistening from horny transformation (Fig. 67). The nucleus 




Fig. 67— Epithelioma of skin, showing concentric arrangement and degeneration of cells. 

may be clear and quite structureless, or may show a distinct 
nucleolus and a definite chromatin network. Karyokinetic fig- 
ures may be quite abundant and are frequently atypical. Degen- 
erative changes (dropsical infiltration, myxomatous change, fatty 
degeneration) may alter the nucleus as well as the body of the 
cell. 

The epithelial cells are usually grouped in the form of acini ; 



PROGRESSIVE TISSUE-CHANGES. 



175 



either completely filled so as to form epithelial clumps or columns, 
or in alveoli with a central lumen surrounded by epithelial cells 
in a number of layers. In the last respect the alveoli differ strik- 
ingly from those of adenoma, and there is the further difference 
that cellular outgrowths may be seen at the periphery of the acini, 
the cells having broken through the retaining wall (basement- 
membrane) and proliferated outside to form new clumps (Fig. 68). 




Fig. 68.— Carcinoma of uterus. 



On examination of the epithelia within the acini it is found that 
those of the peripheral layer frequently retain the columnar char- 
acter seen in the normal alveoli of the gland from which the tumor 
springs. The connective-tissue stroma of carcinoma is more or 
less dense, but practically is always of fibrous character. It is 
arranged in such manner as to form hollowed spaces or columns 
in which the epithelial structures already described are embedded. 
Frequently infiltrating leukocytes and plasma-cells or mast-cells 
are seen within the stroma, and the latter also bears the vascular 
channels that supply the tumor. 

The above description applies to the ordinary carcinoma of 
glandular organs. Differences are observable in the cancers of 
the skin and other external surfaces. In these the structure is 
rather that of much enlarged papillae penetrating into the deeper 
tissues. The cells are similar to those of the deeper layers of the 
skin, are larger than those of glandular cancers, and more translu- 
cent. Hollowed alveoli are exceptional. 

Degenerative Changes. — Carcinomata are quite prone to 



176 



TEXT-BOOK OF PATHOLOGY. 



degenerations. In nearly all cases in which the tumor has reached 
considerable size more or less fatty degeneration of the cells 
becomes apparent. Preceding this or associated with it may be 
cloudy swelling or dropsical infiltration of the cells, rendering the 
nuclear outline less distinct and sometimes causing vacuolations. 
Irregular and multiform nuclear degenerations are met with, and 
probably occasion some at least of the structures known as para- 
sites of cancer. The epitheliomata of the skin are particularly 
prone to a horny transformation, this occurring first and most 
prominently in the concentric whorls already described. In the 
adenocarcinomata of the ovaries and other genital organs of women 
the degenerated epithelial cells frequently undergo calcareous infil- 
tration, and psammomata are thus formed. Colloid degeneration 
of the epithelial cells is a rare event, and the term colloid cancer is 
generally a misnomer, the real degeneration in most of these being 
myxomatous, affecting the connective tissue principally, though 
the epithelial cells are to a certain extent involved. Complete 
degeneration by myxomatous or associated myxomatous and fatty 
change may destroy all of the characteristics of the original tumor. 
In some cases cystic transformation occurs in organs the seat of 
cancer, or in the cancer itself. This may be due to occlusion and 
subsequent dilatation of the ducts of the organ or of the acini in 
the tumor, the cystic spaces becoming filled with mucoid or 
gelatinous material. In some instances cystic carcinomata are 
secondary developments originating in cystic adenomata. Hyalin- 
change and pigmentation are rare in cancer. 

Inflammatory processes are quite common. Cancers on free 
surfaces are prone to undergo ulceration in consequence of irrita- 
tion and infection. Among the micro-organisms discovered in 
such instances the staphylococcus and streptococcus are conspicu- 
ous. A distinct erysipelatous inflammation may occur in cancers 
as in other structures. Invasion of tubercle-bacilli and the 
deposit of miliary tubercles in carcinoma are rare events, though 
they sometimes occur. Associations of carcinoma and tuberculosis 
or syphilis may in other cases result from the secondary growth 
of cancer in pre-existing gummatous or other syphilitic lesions or 
in lupus. Practically all carcinomata show some leukocytic infil- 
tration. The amount of this, hoAvever, varies greatly. 

Nature. — Carcinoma is essentially malignant, the degree of 
malignancy depending, however, upon the seat and upon certain 
peculiarities of the individual. Sometimes a small growth may 
remain practically latent for a long time until accidental circum- 
stances, like traumatism, intercurrent disease, pregnancy, or the 
like, stimulate active growth. 

Carcinoma exhibits all the elements of malignancy : the ten- 
dency to recur after removal, metastasis, and general destruction 
of the health. Recurrence after removal is most readily explained 



PB GRESSI VE T1SS UE-CHANGES. 



177 



upon the assumption that the entire growth has not been re- 
moved. Microscopic studies show that the area of infiltration is 
usually much greater than the naked-eye appearances would indi- 
cate, and this explains why the surgeon cannot well remove the 
whole disease. Metastasis, as a rule, follows the lymphatic chan- 
nels, and thus primarily involves the lymphatic glands in the 
neighborhood of the growth. The process may be explained as 
follows : some of the epithelial cells in their advancing prolifera- 
tion penetrate the lymphatic channels and are carried in the 
lymph-stream to the nearest lymphatic gland, where they again 
proliferate and form secondary nodules ; from these a similar 
extension occurs, and eventually widespread metastasis results. 
Less frequently the primary growth penetrates the walls of a vein 
and metastasis occurs through the circulation. This is quite com- 
mon in the case of cancers of the stomach or intestines. The 
metastatic foci first spread through the portal circulation to the 
liver. In still other instances secondary growths result from 
mechanical transportation in the movements of the body ; thus 
in carcinomata of the abdominal organs the peristaltic move- 
ments may transfer particles to different parts of the abdominal 
cavity. 

Pathologic Physiology. — The general health of patients suffer- 
ing with carcinoma is affected very profoundly, though the man- 
ner in which this occurs remains obscure. It would seem to be 
of the nature of a toxemia. Emaciation and loss of strength are 
habitual, though often, perhaps, in large part the result of inter- 
ference with organic functions, as, for example, in carcinoma of 
the stomach. Progressive anemia may make its appearance, the 
red corpuscles becoming less abundant and the quantity of hemo- 
globin falling decidedly. There is usually a moderate amount of 
leukocytosis, the large mononuclear forms increasing particularly. 
Toward the end of life the tissue-destruction increases greatly, 
though the excretory products of such may not be notably in- 
creased in the excretions in consequence of failing circulation and 
imperfect renal function. At this stage the accumulation of such 
products in the blood may lead to sudden death from coma (see 
Acid-intoxication). Hemorrhages and ulcerations may also con- 
tribute to the impairment of health in cases of cancer. 

Varieties of Carcinoma. 

There are several forms of cancer sufficiently different to re- 
quire separate description. The classification of these is generally 
based upon the character and arrangement of the epithelium. We 
may distinguish (1) carcinomata composed of surface-epithelium, 
either (a) squamous or (6) cylindrical, and (2) glandular carcino- 
mata, having either (a) more or less distinct adenomatous structure 

12 



178 



TEXT-BOOK OF PATHOLOGY. 



or (b) solid plugs or columns of epithelial cells, or (c) a mixture 
of acini and solid columns. 

Epithelioma. 

This form, which consists of surface-epithelium, is of two 
varieties, the squamous and the cylindrical. 

Squamous epithelioma occurs in the skin or mucous mem- 
branes, where squamous epithelium exists normally. Among the 
frequent seats are the lips, the esophagus, the larynx, and the cer- 
vix uteri. Occasionally squamous epithelioma arises in parts nor- 
mally covered by other kinds of epithelium ; as, for example, in 
the fundus of the uterus. In these instances there is probably a 
primary metaplasia of the epithelium followed by carcinomatous 
growth. Squamous epitheliomata present themselves as nodular, 
wart-like elevations of the skin or mucous membrane, tending to 
become ulcerated on the surface. Those of the mucous surfaces 
are more elevated and softer. Histologically there are seen branch- 
ing columns of epithelial cells extending downward from the pa- 
pillae of the skin into the deeper structures. These consist of 
large translucent squamous cells which show a tendency to arrange 
themselves in certain places concentrically to form epithelial 
perles. The latter frequently undergo a horny transformation 
and sometimes even calcareous change (Fig. 69). The same 




Fig. 69.— Squamous epithelioma, showing whorls of epithelial cells with central degen- 
eration (from a photograph by Dr. W. M. Gray). 

structures occasionally occur in benign papillomata, but much less 
frequently. Metastasis is frequently seen in the neighboring 
lymphatic glands, but the malignancy is less marked than in 
glandular carcinomata. 

Cylindrical Epithelioma. — This form is composed of co- 
lumnar or cylindrical epithelium. It is frequent in the mucous 
membranes, especially in the gastro-intestinal tract and the uterus. 



PROGRESSIVE TISS UE-CHANGES. 



179 



The epithelial cells of the tubular glands or sometimes those 
of the surfaces form the starting-point of the growth. More 
or less acinus-like tubular structures, composed of a layer of 
epithelial cells, or more frequently of a number of layers of epi- 
thelia, the outer layer being often distinctly columnar, constitute the 
characteristic feature of the tumor (Fig. 70). In the later stages 




Fig. 70.— Cylindrical epithelioma of the intestine (Perls'. 



the acini become filled with proliferated epithelial cells of various 
shapes and the cylindrical or tubular character of the acini is lost. 
Carcinomata of the kidney, liver, and mammary gland, though not 
originating from surface-epithelium, strictly speaking, may be of 
the cylindrical form. Cylindrical epitheliomata more nearly 
resemble the glandular carcinomata in their malignancy and 
general behavior than the squamous variety. 

Glandular Carcinoma. 

This term includes the carcinomata that have a resemblance 
to racemose glands in their histologic structure. They consist 
of acini or alveoli containing epithelial cells, usually in several 
layers or completely filling the lumen, and a stroma of connective 
tissue. Some authors distinguish three forms : the simple, the 
medullary, and the scirrhous. These are simply variations of the 
same tumor. In the simple form there is a combination of epi- 
thelium and stroma in about the proportion seen in normal glands. 
The tumor is therefore neither strikingly hard nor soft. In the 



180 



TEXT-BOOK OF PATHOLOGY. 



medullary or soft carcinoma the amount of epithelium is excessive 
and the tumor has a soft character (Fig. 71); while the scirrhous, 




Fig. 71.— Medullary carcinoma of breast. 



or hard, cancer is an indurated form, due to excess of fibrous tissue 
and deficiency of the epithelium (Fig. 72). 

The glandular cancers are more or less nodular or infiltrating 




Fig. 72.— Scirrhous cancer of breast (Warren). 



growths varying in consistency in different cases, but having on 
section a glistening white color with a certain amount of translu- 



PE GRESSI VE TISS UE-CHANGES. 



181 



cency. Milky liquid exudes from the surface on section. This 
is composed of albuminous fluid containing degenerated epithe- 
lium and free oil-droplets. Among the seats in which these forms 
occur the most important are the pylorus and other mucous sur- 
faces, the mammary gland, the pancreas, kidneys, ovaries, and 
testicles. Widespread metastasis and other features of malignancy 
are noted. In the case of the scirrhous form the primary tumor 
may be strikingly small in comparison with the amount of meta- 
static deposit. 

Colloid Cancer. 

This term is usually a misnomer, as most of the colloid cancers 
contain no colloid material. The name gelatinous would be more 
appropriate, but has not been generally accepted. Colloid cancers 
are met with in the stomach and intestinal tract, in the mammary 
gland, and in the ovaries. The tumor has a peculiar transparent, 
glistening appearance. The entire mass may be uniformly jelly- 
like, or only portions of it are affected. Microscopically mucous 
degeneration of the connective tissue as well as of the epithelial 
cells is discovered (Fig. 73). In some cases no trace of carcinom- 




Fig. 73.— "Colloid cancer" of the breast, showing myxomatous change in the stroma and 
fatty degeneration and partial disappearance of the epithelial cells (Perls). 

atous tissue may be discoverable, the whole tumor having under- 
gone degeneration. Sometimes the process involves the epithelium 
rather than the connective tissue. Colloid cancers frequently spread 
by direct extension, and the entire abdominal cavity may become 
filled with gelatinous material, representing degenerated secondary 
growths. Occasionally the same kind of peritoneal growths seem 
to originate primarily in the peritoneum, springing from fetal rem- 
nants of epithelial tissue (Fig. 74). 

True colloid cancer — that is, carcinoma with colloid degenera- 
tion of the epithelium — is sometimes seen, though it is very rare. 
It occasionally causes a gross appearance resembling that of sar- 



182 TEXT-BOOK OF PATHOLOGY. 

coraatous cylindroma, and the term carcinomatous cylindroma has 
been applied. 




Fig. 74.— Colloid cancer of the peritoneum (modified from Birch-Hirschfeld). 

SYNCYTIOMA MALIGNUM. 

This term is applied to a form of tumor originating at the 
placental site during pregnancy or the puerperium. It has also 
been called deciduoma malignum, sarcoma deciduocellulare, 
destructive epithelial tumor of the placental site, and chorio- 
epithelioma. 

The tumor occurs as a hemorrhagic infiltrating growth, some- 
what resembling placental tissue in gross appearance, and fre- 
quently gives metastasis by breaking into the blood-vessels. The 
metastatic nodules are found in the external genitalia, frequently 
in the lungs, less often in the liver, spleen, or other organs. The 
growth is rapid, the uterine Avail being quickly invaded and met- 
astasis occurring in a short time. 

The nature of this tumor is still the subject of some contro- 
versy. Two types of cellular elements are recognized in its struct- 
ure. One of these consists of irregular masses of protoplasm con- 
taining dark nuclei. The nuclei probably multiply by direct 
division. These protoplasmic masses are arranged in islands or 
in branching columns which form a network. In the meshes of 
this network are blood-spaces containing thrombi or masses of 
blood-corpuscles. Sometimes masses like those above described are 
found within the blood-spaces. The second form of cells consists 



PROGRESSIVE TISSUE-CHANGES. 



183 



of smaller irregular-shaped elements, which are unusually rich in 
glycogen, and in which cell-division by karyokinesis is observed. 
These cells lie in masses, of greater or less size, between and beside 
the larger protoplasmic areas before described. In the later stages 
of the growth obliterative thrombosis of the vessels leads to necro- 
sis of the cellular constituents, particularly of the columns of large 
epithelium-like cells. These are converted into homogeneous 
fibrinous masses, and even the thrombi themselves may degen- 




Fig. 75.— a, Fibrin, with numerous small round cells caught in the meshes ; b, cells 
resembling decidual cells, probably a proliferation of the Langhan's cells ; d, protoplasmic 
masses containing large free nuclei. 

erate. The view of Marchand regarding the nature of these 
tumors is most widely accepted. He holds that the larger cells 
are derivatives of the syncytium (a structure composed of epithe- 
lial cells, probably of fetal origin), while the smaller cells are 
formed from the epithelial covering of the chorion villi (Langhan's 
cells). The tumor, therefore, is epithelial in nature, and it has 
malignant properties. It differs, however, from ordinary epithe- 
lioma and from carcinoma in its peculiar structure and in its clin- 
ical course and dissemination. 

CYSTS. 

Definition. — This term includes pathologic formations of 
varied character. Some are true tumors ; others are of quite dif- 
ferent nature. 

The term cyst is applied to pathologic formations consisting of 
a more or less well-defined wall and enclosing liquid or semiliquid 
contents of different character from the surrounding parts. This 
definition is not entirely applicable, as certain structures that do 



184 



TEXT-BOOK OF PATHOLOGY. 



not present a definite capsule are sometimes termed cysts. Ac- 
cordingly we may distinguish between true cysts and cyst-like 
formations or cystoids, the former being enclosed by a capsule 
lined with epithelium or endothelium ; the latter merely present- 
ing a circumscribed collection of softened material. 

Classification. — According to the method of formation, we 
distinguish retention-cysts, softening-cysts, cysts due to the pres- 
ence of foreign bodies, and proliferation-cysts. 

Retention-cysts are formed when the excretory ducts of a gland 
become occluded and the secretions accumulate and cause disten- 
tion of the acini or of parts of the duct. Among such cysts may 
be named the distended sebaceous glands of the skin in the forma- 
tions called wens; the cysts of the salivary or small mucous 
glands or ducts under the tongue, called ranulce ; retention-cysts 
formed in the uriniferous tubules, the tubules of the ovary, or in 
the parovarium, in the acini and ducts of the mammae, pancreas, 
and other glands. An entire organ may become converted into a 
cyst, as in cases of distention of the kidney (hydronephrosis) from 
obstruction of the ureter. 

These cysts are distinguished by the fact that they have a dis- 
tinct connective-tissue wall lined with epithelium or endothelium. 
The contents of the cyst depend upon the part in which the forma- 
tion has taken place. 

Softening-cysts occur in consequence of degenerative softening 
of normal or pathologic tissues. They are not rarely the result 
of hemorrhage, the blood-clot first becoming inspissated and then 
serous exudation occurring in the area of hemorrhage. Softening- 
cysts are very common in tumors of different kinds. 

Cysts due to foreign bodies are in part softening-cysts. The 
tissues in the immediate vicinity may be injured and undergo 
necrotic softening, while connective-tissue reaction produces a 
capsule. This form of cyst is most frequently the result of in- 
vasion of parasites, and the cyst-contents may be composed of 
the parasite or the parasite and tissue-elements more or less 
degenerated. 

Proliferation- cysts. — This term is applied to formations more 
closely analogous to true tumors than those mentioned before. 
They merit more extended description than the other forms of 
cysts, and may be designated as epithelial cysts. 

Epithelial Cysts. 

Definition. — In certain glandular organs, notably the ovary 
and mammary gland, cystic formations occur which present strik- 
ing appearances ; and though perhaps they represent adenomatous 
or carcinomatous new growths, are so striking as to deserve special 
mention. 



PROGRESSIVE TISSUE-CHANGES. 



185 



Etiology. — These growths, in part at least, result from ob- 
struction of excretory ducts and subsequent irritation by retained 
secretions. Congenital abnormalities of structure may possibly 
play a part in their causation. 

Appearance. — Cystomata may be single or multiple, the 
entire tumor being composed either of a single cyst or of one large 
cyst subdivided into many smaller, or again of numerous separate 
and unconnected cysts of varying size. On section the cystic 
cavities are found to contain more or less serous or gelatinous 
liquid, and sometimes hemorrhagic fluid is observed. Most fre- 
quently the liquid is gelatinous or ropy, and is commonly spoken 
•of as colloid material. The inner lining of the cyst may be 
smooth, like a serous or mucous surface, or elevated irregularly in 
the form of polypoid outgrowths into the cavity of the cyst. The 
entire cyst may thus be filled with papillomatous elevations from 
the epithelial lining. The term papuliferous or proliferative cyst- 
omata is given to these forms (Fig. 76). The size of cystomata 




Fig. 76. — Papuliferous adenocystoma of the kidney (Karg and Schmorl). 

varies from minute tumors not larger than a pea to enormous 
masses weighing as much as sixty or eighty pounds. Secondary 
degenerations may occur in the form of softening, hemorrhage, or 
calcification. 

Seats. — The mammary gland and ovary are the principal 
situations in which tumors of this description are met with, but 
analogous growths may make their appearance in any of the 
glandular organs. 

Structure. — Microscopically these growths present cystic 
cavities lined with typical or modified columnar epithelium and a 
stroma or reticulum of connective tissue. The amount of the 



186 



TEXT-BOOK OF PATHOLOGY. 



latter and the appearance of the cysts themselves vary in different 
cases. At times the stroma is very abundant and takes the form 
of well-organized fibrous tissue, while the cysts and acini are small 
and few in number. In these cases the appearance suggests a 
primary proliferative connective-tissue process with secondary 
implication of the epithelial elements. Such cases occur particu- 
larly in the mammary gland, and there is difficulty in separating 
them sharply from instances of chronic interstitial mastitis or dif- 
fuse fibroma. In other instances the process manifestly begins 
with the formation of epithelial acini, and the hyperplasia of 
the connective tissue is certainly secondary. The acini in these 
cases present themselves as hollow spaces of varying shape and 
size, often branching, and lined with columnar epithelium in a 
single layer or sometimes with several layers of more or less dif- 
ferentiated columnar epithelium. 

Nature. — These cystic growths often have a decided tendency 
to malignancy. They may remain benign throughout; but fre- 
quently they undergo carcinomatous change and spread widely or 
give rise to metastasis. The malignancy is generally in propor- 
tion to the amount of the epithelial proliferation and papuliferous 
change, but there are instances in which metastasis occurs from 
adenocystomata having regular gland-acini lined with single layers 
of typical columnar cells. The cystomata of the ovary not rarely 
extend to the surface of the organ, break through the capsule, and 
present upon the surface as papillary growths, and frequently 
they extend to the peritoneum and neighboring structures. The 
entire abdomen may be involved. At the same time, or in other 
cases independent of such direct extension, metastatic deposits 
may be seen in nearby lymphatic glands. Somewhat the same 
conditions may be observed in cystoma of the breast, but in this 
situation the tumor is much more frequently confined within the 
capsule of the organ. 

TERATOMA. 

Definition. — The term teratoma is applied to tumors of pecu- 
liar mixed character, representing different elements of complex 
tissues or structures in a situation in which these do not normally 
occur. For example, the most frequent form of teratoma contains 
various epidermal structures, such as hair, teeth, etc., and occurs 
in internal organs. 

Etiology. — The causation of teratoid tumors or teratomata is 
to be sought in congenital misdevelopments. We may, with Klebs, 
distinguish endogenous forms, in which inclusions of superficial 
tissues are retained in internal parts by a process of constriction ; 
and ectogenous forms, in which a separate fetal deposition is the 
origin of the tumor. The latter form represents a separate and 



PROGRESSIVE TISSUE-CHANGES. 



187 



ill-developed fetus within the developed organism — a fetus infetu. 
A regular gradation may be traced from distinct teratoid tumors 
having irregular mingling of tissue-elements, to malformations in 
which a more or less systematic outgrowth, somewhat approaching 
double monstrosities, occurs. Of the distinct teratoid tumors the 
most frequent is the dermoid cyst. 

Dermoid Cyst. 

This tumor presents itself as a cystic formation with a con- 
nective-tissue membrane and an inner lining resembling the skin. 
This may present all the elements of the skin, such as stratified 
epidermis, a papillary layer, and even subcutaneous connective 
tissue. Hair-follicles and sebaceous glands are frequent, and 
habitually long, light-colored hairs are found within the contents, 
and teeth may be found in the lining membrane or free in the 
contents of the cyst. The cyst is filled with a semifluid, cheesy 
mass consisting of epithelial cells, fatty matter, and other detritus. 
Occasionally dermoid cysts may contain nerve-tissue, muscle, or 
structures resembling intestine. 

The dermoid cysts vary in size from minute bodies no larger 
than a pea to huge masses, the latter being most frequent in the 
ovaries. Among the situations in which dermoids occur the 
ovaries are most common ; less frequently they are found in the 
testicles, in the peritoneum, in the membranes of the brain, about 
the eye, in the neck, floor of the mouth, and elsewhere. Growth 
is very slow, and they may remain practically latent through life. 

The nature of these tumors is usually benign, though carcinom- 
atous change may occur, and in the ovaries cystoma is prone to 
be associated, and the latter may be malignant. 

Other Teratoid Tumors. 

Nodular masses may appear about the head or neck or in vari- 
ous parts of the body, consisting of mingled tissues of various 
kinds, such as glandular tissues, connective tissues, nerve, mus- 
cle, etc. These can be classified as teratoid growths. Sometimes 
they resemble some definite organ, as in the case of growths 
appearing at the umbilicus of the new-born and simulating the 
structure of normal intestine. 

In the neck there are sometimes seen more or less cystic 
growths lined with epithelium and having in their walls muscle- 
fibers, lymphoid tissue, cartilage, etc. These growths probably 
spring from remnants of the embryonal branchial clefts. The 
mixed tumors of the parotid gland (see Sarcoma) are allied to 
these. 

Cholesteatoma. — This tumor is characterized by glistening, whit- 
ish, or pearly bodies composed of concentric layers of cells resem- 



188 



TEXT-BOOK OF PATHOLOGY. 



bling epithelium (Fig. 77). Sometimes crystals of cholesterin are 
found in the center of these bodies, whence the name choles- 
teatoma. Cholesteatomata are found in the membranes or sub- 
stance of the brain, and present themselves as single or multiple 
nodules. They are usually soft and glistening in appearance. 



/ 




Fig. 77. — Cholesteatoma from the membranes of the brain. 



Some authors consider them endotheliomata, but Ziegler has 
found hair-follicles and hairs in certain specimens, and from this, 
as well as from the horny change to which the cells in the pearly 
bodies are prone, classifies them among the teratoid growths. 

Somewhat similar tumors occur in the pelvis of the kidneys, in 
the testicles, parotid glands, ovaries, and middle or external ear. 



CHAPTER VII. 

BACTERIA AND DISEASES DUE TO BACTERIA. 

History. — Although for many centuries there had existed the 
idea that disease and decay are due to the action of minute or- 
ganisms, it was not until the use of the lens enabled the Dutch 
naturalist Leeuwenhoeck actually to demonstrate their presence in 
water and in human intestinal contents that the hypothesis of a 
" contagium vivum " became more than mere guesswork. He 
discovered, even with his imperfect instruments, short rods, curved 
and straight, and described their motility. Miiller (1785), by the 
use of the compound microscope, attempted a more systematic 



BACTERIA AND DISEASES DUE TO BACTERIA. 189 



classification of these micro-organisms, and from this time many 
investigators have added much to our knowledge of microbes, 
that group of organisms which had been denominated by Linnaeus 
by the term Chaos. To the German Henle is due the credit of 
having first introduced an idea of order into this disorder. He 
held that fermentation was the result of organic life, and that the 
action of a contagium was analogous to that of a ferment. The 
earliest systematic experimental work was that of Pasteur, in which 
he established beyond doubt this relation between fermentation 
and the life and development of bacteria. The first definite ideas 
of the physiology of these micro-organisms are found in his experi- 
ments on lactic-acid fermentation, and those of their pathogenesis, 
in his demonstration of the microbic origin of the silkworm-disease 
(1869). Davaine and Rayer about the same time established the 
causal relation of a bacillus found in the blood of a sheep dead 
of anthrax to that disease. 

CLASSIFICATION. 

Bacteria (schizomycetes, or cleft fungi) is the name given to a 
branch of the lowest and simplest of the orders of the vegetable 
kingdom. They are small, unicellular organisms, generally free 
of chlorophyll, and colorless ; they possess a cell-membrane albu- 
minoid in composition and homogeneous protoplasmic cell-contents. 
Some varieties are motile. Nuclei are absent, though in the opin- 
ion of some the whole body may be regarded as a nucleus. Bac- 
teria multiply by cell-division, sexual distinctions being absent. 
In many species resistant forms — spores — occur. 

The simple elementary forms that occur are of three kinds : 
the coccus, the bacillus, and the spirillum (Fig. 78). 




Fig. 78— Various forms of bacteria: 1 and 2, round ahd oval micrococci; 3, diplococcl ; 
4, tetracocci, or tetrads ; 5, streptococci ; 6, bacilli ; 7, bacilli in chains, the lower showing 
spore-formation; 8, bacilli showing spores, forming drumsticks and Clostridia; 9 and 10, 
spirilla ; 11, spirochete. 

COCCUS. — This is a spherical cell, varying in size up to 1 in 
diameter. It takes the anilin-stains readily. Spore-formation 
and motility are rare. When the cocci are found in groups, the 
individuals being entirely separate, they are termed staphylococci, 
from the resemblance of the groups to a bunch of grapes ; when 
in pairs, diplococci ; when in chains, streptococci ; when in groups 
of four, tetrads or merismopedia ; when in packets, sarcinse. 

Bacillus. — A rod-shaped, cylindrical cell of varying length 
and thickness. Spore-formation and motility are common. Most 



190 



TEXT-BOOK OF PATHOLOGY. 



of the group stain easily with the anilin dyes, but some require 
special methods of staining. 

Spirillum. — A cylindrical, rod-shaped cell, curved or spiral, 
sometimes motile. It stains readily. 

Many other classifications, all of them being to a certain extent arti- 
ficial, have been made by different authors. Probably one of the most 
useful and scientific is that of Migula: 

I. Coccaceae. — Spherical cells dividing in one, two, or three directions. 

Endospores rare. 

1. Streptococcus. — Division in one direction, the individuals cohering 

to form chains. Motility absent. 

2. Micrococcus. — Division in two directions, the individuals when 

coherent forming groups of four. Flagella absent. 

3. Sarcina. — Division in three directions, forming packets of eight, 

twenty-seven, or more cells. Motility absent. 

4. Planococcus. — Division in two directions, as in the micrococcus. 

Motility present. 

5. Planosarcina. — As the sarcina. Motility present. 

II. Bacteriaceae. — Rod-like, cylindrical cells, dividing at right angles to 

the long axis. 

1. Bacterium. — Cells without flagella, often with spores. 

2. Bacillus. — Cells with peritrichous flagella, often with spores. 

3. Pseudomonas. — Cells with polar flagella ; spores rare. 

III. Spirillacese. — Cells cylindrical, curved, bent, or spiral. Division as 

in II. 

1. Spirosoma. — Cells rigid, without flagella. 

2. Microspira. — Cells rigid, with one, rarely two or three, polar flagella. 

3. Spirillum. — Cells rigid, with five to twenty polar flagella. 

4. Spirochete. — Cells flexible, motile, but without flagella : perhaps 

possessing an undulating membrane. 

IV. Chlamydobacteriacese. — Cells united in a simple unbranched fila- 

ment. Division in one direction. Forms non-motile; conidia. 

1. Streptothrix. — Cells united in a simple unbranched filament. 

Division in one direction. Forms non-motile ; conidia. 

2. Cladothrix. — Cells united in a filament, with a false branching. 

3. Crenothrix. — Cells united in an unbranched filament, and dividing 

in three directions into small rounded cells. 

4. Phragmodiothrix. — Cells at first united in an unbranched filament, 

and dividing in three directions. Later the separate cells break 
through the thin membrane and grow out as branches. 

5. Thiothrix. — Cells united in an unbranched filament contained in a 

thin membrane. Division in one direction. Cells contain gran- 
ules of sulphur. 

V. Beggiatoacese. — Cells united in a filament without sheath. Motile, the 

movement being due to an undulating membrane. 



MORPHOLOGY. 

Cell -contents. — The body of the organism in unstained con- 
ditions appears as a perfectly homogeneous protoplasmic mass. On 
staining with anilin dyes a granular appearance is often observed, 
which under high powers is resolved into a hyaline mass contain- 
ing numerous chromophilic granules. Vacuolations also are often 



BACTERIA AND DISEASES DUE TO BACTERIA. 191 



present. Some modern observers (Butschli et al.) have made out a 
network immediately within the membrane and surrounding a 
central body which readily stains with the nuclear dyes. This 
latter they regard as a nucleus. Others, however/ affirm that this 
appearance is due to a concentration of the cell-protoplasm (endo- 
plasm), the result of the rather complicated method of staining. 
The question of the presence or absence of a nucleus is still an 
open one. In many organisms, as the Bacillus diphtheria? from a 
blood-serum culture, for example, there exist certain transparent 
refractive bodies which stain differently from the rest of the 
microbe. These metachromatic bodies, as they are called, were 
regarded by Ernst as nuclear in character. Others look upon 
them as possibly the primary state of spore-formation. 

Spore. — The spore is a non-vegetative resistant form that the 
microbe assumes when the conditions for growth are unfavorable. 
The endoplasm seems to concentrate and become a small, oval, 
highly refractive body, separated from the bacterial protoplasm by 
a membrane of its own. It is generally of the same diameter or 
somewhat smaller than the bacillus itself, and is situated either in 
the middle (equatorial) or at the end of the microbe (polar spore). 
It may be larger in diameter than the microbe and cause a swell- 
ing at that point. When in the center of the rod this gives rise 
to the form known as Clostridium ; when polar, to the so-called 
drumstick-form (as in the Bacillus tetani). 

Such intracellular spores or endospores occur among many 
bacilli. Among the micrococci they are rare ; but it is supposed 
that certain individual cocci become larger and more refractive in 
appearance and assume the spore-state. These are called arthro- 
spores. Whether these can be regarded as true spores is still 
doubtful. 

The spore is extremely resistant to conditions to which the 
vegetative form readily succumbs ; to the action of certain chemi- 
cal reagents, light, heat, etc. Bacteria that are grown on media 
poor in nutrient material tend to become asporogenous. A certain 
temperature is also necessary for spore-formation. Thus, although 
the anthrax bacillus develops well at a temperature of 14° C. 
(57° F.), it does not form spores below 18° C. (64° F.). To obli- 
gate aerobes oxygen is necessary for their development, and anae- 
robic cultures present them only in the absence of that gas. 
Placed under conditions favorable to its vegetation the spore loses 
its clearness, absorbs water, and swells. A small prominence pre- 
sents at the side or end, which gradually lengthens and develops 
into a young bacillus. The membrane of this new microbe is 
formed from the inner layer of the spore-membrane (endosporium), 
while the outer layer (exosporimn) is cast off. In not all of the 
varieties of bacilli does sporulation take place, and even where it 
does occur there may, under certain conditions, as in growth at 



192 



TEXT-BOOK OF PATHOLOGY. 



high temperatures, arise races which have lost this power (aspo- 
rogenous races). 

The spore does not stain readily with the ordinary anilin 
stains, and special methods have been devised for coloring it. 

Cell-membrane. — Surrounding each organism is a membrane 
(ectoplasm) denser and more highly refractive than the cell-con- 
tents (endoplasm). In some cases this is not to be differentiated 
from the endoplasm ; but in others it is larger, and under certain 
conditions becomes a gelatinous mass. In this case it is easily 
seen, especially after appropriate staining. This is called the 
capsule. In general this occurs only when the bacteria develop 
within the animal organism, and not upon artificial culture-media. 
It is probable that the ectoplasm is not a mere protective envelop, 
but has to do with the functional activity of the bacterium. The 
fact that the flagella, to which is due the motility of certain mi- 
crobes, are directly continuous with and are simply prolongations 
of this membrane, points to this view. 

The cell-membrane is not easily colored by ordinary methods. 

Flagella. — Motility is often a property of bacteria. It is 
manifested in different ways, and is often characteristic of the 
several varieties of bacteria. Some move slowly forward across 
the field, others with great rapidity ; others again dart hither and 
thither, slowly or so quickly as to be with difficulty observed. 
They may at the same time have a rotary movement around their 
long or their short axes. 

After appropriate staining the cause of this motility is seen to 
be the presence of slender, whip-like prolongations, originating 
directly from the ectoplasm (Babes). They may be twenty times 
as long as the body of the bacterium, and are arranged in the dif- 
ferent species in different ways. Bacteria that possess no flagella 
are termed Gymnobacteria ; those that have these organs, 
Trichobacteria. There may be but one flagellum, situated at the 
pole (memoir ichous), or a number may be present (lophotr ichous).' 
When they are situated at both poles the microbe is termed amphi- 
tr ichous ; when distributed over the whole body of the bacteria, 
peritrichous. The presence and the activity of flagella depend on 
many factors : on the condition of the medium, bacteria grown from 
liquid media being more active than those from solid ; on tem- 
perature ; on presence of air ; on light ; and on the age of the 
culture. They are easily broken off from the microbe, and care 
must be used in staining them. A special method is employed. 

Involution-forms. — By involution-form is meant the irreg- 
ular appearance a microbe often assumes when its conditions of 
growth are unfavorable. Numerous bacteria melt together and 
become irregular chains, or they appear pear- or club-shaped. 
The protoplasm becomes retracted and irregular staining takes 
place. Sometimes the microbes lose all characteristic appearances. 



BACTERIA AND DISEASES DUE TO BACTERIA. 193 



Sometimes forms with branching projections are discovered. 
These have often been described as involution-forms, but are now 
more commonly regarded as normal, though unusual, structures. 
This applies to tubercle bacilli, diphtheria bacilli, and some 
others. This true branching (dichotomy) must not be confounded 
with false or pseudodichotomy, due to mere apposition of separate 
organisms, as seen in various bacilli, streptococci, etc., and habitu- 
ally in the cladothrices. 

Chemistry. — The bacterial cells are of variable composition, 
depending to a great extent upon the kind of nutrient matter. It 
consists mainly of water (85 per cent.). The chief solid material 
is albumin. This varies according to the medium of growth, and 
has been given the general name of mycoprotein (Nencki). Fat 
is also present. The nuclein-bases, xanthin, guanin, adenin, and 
cellulose, have been found by some. Some contain certain color- 
ing-matters, bacteriopurpurin and a green substance similar to 
chlorophyll. Organic acids and ferments of different kinds are 
also found. In some special forms — the sulphur bacteria — sul- 
phur is present. 

DEMONSTRATION. 

The success of the microscopic examination of bacteria in 
the several fluids and tissues of the diseased body and in pure 
cultures depends upon the differentiation of the microbes from the 
surrounding substances by certain chemical reagents. The process 
is twofold : to render more transparent the non-bacterial elements 
and to render more visible the bacteria themselves. Thus a 1-^- 
per cent, solution of sodium hydrate dissolves the histologic ele- 
ments except the fatty, elastic, pigmentary, and amyloid substances 
and bacteria. 

Methods of this sort have been entirely superseded by the use 
of the anilin dyes. AVe can with these render bacteria more visi- 
ble and at the same time differentiate them from the surrounding 
tissue by means of contrast- or counter-stains. 

Microbes, generally, stain with dilute aqueous or alcoholic 
solutions of the anilin colors, but they differ greatly in the readi- 
ness with which they take the stain and the tenacity with which 
they hold it after treatment. To stain some it is necessary to 
employ heat or to add some chemical substance to act as a mor- 
dant and enable the stain to pass through the cell-membrane. 
The most important of these are potassium hydrate, anilin oil r 
alcohol, carbolic acid (1-5 per cent.), acetic acid (0.5-1 per cent.). 

Some bacteria decolorize easily, even with water ; others 
can be placed in alcohol, and some in strong solutions of mineral 
acids, without losing their color. Those bacteria that stain easily 
are the most readily decolorized. 

13 



194 



TEXT-BOOK OF PATHOLOGY. 



Among the more frequently used of the anilin dyes are : 
methylene-blue, dahlia, fuchsin, vesuvin, gentian-violet and thi- 
onin. The following are useful formulae : 

Loffler's methylene-blue : 

Saturated alcoholic solution of methylene-blue . 30 cc. 
Aqueous solution of potassium hydrate (0.01 



per cent.) 100 cc. 

Carbolized thionin : 

Saturated alcoholic solution of thionin . . . . 10 cc. 
Carbolic-acid solution (1 per cent.) 100 cc. 



Bacteria stained with these upon cover-glasses need no after- 
treatment; but tissues are to be decolorized with alcohol. With 
Loffler's solution the decolorization must be stopped at a point 
where the protoplasm is colorless and the nuclei are faintly stained. 
The bacteria remain a bright blue. Bacteria stained with thionin 
retain a reddish tinge, however, even after prolonged action of 
the alcohol. 

ZiehVs solution is the best known stain for the Bacillus tuber- 



culosis : 

Fuchsin 0.25 gm. 

Alcohol 10 cc. 

Carbolic-acid solution (5 percent.) 100 cc. 



Treated with this for some three to five minutes (for tissues 
longer) and with heat, the bacilli retain their red color after the 
use of strong mineral acid solutions (sulphuric, nitric, or hydro- 
chloric acid, 25 per cent.). A counter-stain, to color the decolorized 
cellular elements, is used, and methylene-blue is generally em- 
ployed. Gabbett mixes the contrast-stain with the sulphuric-acid 
solution. 

Gram's Method. — Another important differential stain is that 
devised by Gram. The specimen is treated for some minutes in 
an anilin- water solution of gentian-violet. Anilin-oil (4 cc.) is 
well shaken up with 100 cc. of distilled water, filtered, and to this is 
added 1 cc. of saturated alcoholic solution of the violet. The 
specimen, stained a few minutes with this, is treated with an 
iodid-iodin solution (iodin, 1 gm. ; potassium iodid, 2 gm. ; water, 
300 cc), which fixes or in some way modifies the stain in the 
bacteria and decolorizes other elements. The further action of 
alcohol decolorizes certain varieties of bacteria stained in this, 
while others it leaves unchanged. Bacillus anthracis, tuberculosis, 
tetani, leprae, diphtheria?, rhinoscleromatis ; Staphylococcus aureus, 
albus, and citreus ; Streptococcus pyogenes ; Pneumococcus ; 



BACTERIA AND DISEASES DUE TO BACTERIA. 195 



Micrococcus tetragenus ; and Actinomyces hominis arc the most 
important species that retain the stain. The Gonococcus ; Bacil- 
lus pneumoniae, typhi abdominalis, coli communis, mallei ; and 
Spirillum choleras Asiatics are among those that are decolorized. 

Staining sections is more difficult : it takes longer time and 
must often be aided by heat. This results in overstaining, and 
decolorization is necessary. Many substances have the power 
of decolorizing the tissue-elements in the following order : the 
first to lose the color is protoplasm, then the nuclei, and lastly 
the bacteria. For such differential decolorization alcohol, anilin 
oil, or acid alcohol is the most used, the point aimed at being to 
stop the decolorization as soon as the nuclei have begun to lose 
their color. Some stains are not removed by this means, as 
Gram's and thionin. 

To stain spores, the specimen is fixed by passing through the 
flame and then put for a half to one hour in fuchsin, either an 
aqueous or alcoholic solution, or in ZiehPs solution. The bacterial 
protoplasm is then decolorized by alcohol or very dilute nitric acid 
and counter-stained with Loffler's blue. 

The capsule is colored with Ziehl's stain and the cell-contents 
decolorized Avith dilute acetic acid (1 drop to 5 cc. of water). 
Ribbert saturates with dahlia the following : distilled water, 100 
cc. ; alcohol, 50 .ee. ; acetic acid, 12.5 cc), and stains but a few 
seconds. A very useful method is to stain the bacilli Avith 
Loffler's blue for a few minutes and Avash for the same time with 
anilin-gentian-A T iolet. The bacilli are blue against a reddish back- 
ground, the capsule standing out uncolored. This is especially 
useful in staining sputa. 

Flagella are still more difficult to stain. The cover-glasses 
must be carefully cleansed from all dust and grease. After fixa- 
tion they are treated with a mordant Avhile hot : 

Aqueous solution of tannin (20 gm. to 80 cc.) . . 10 cc. 

Aqueous solution of ferrous sulphate 5 cc. 

Alcoholic solution of fuchsin 1 cc. 

The stain is a saturated solution of fuchsin in anilin-Avater. As 
used by Loffler, a certain quantity of alkali or acid is added to 
the mordant, according to the species of bacteria, but this has 
been found to be unnecessary. 

BIOLOGY. 

Bacteria may be divided into tAvo great classes : those that 
live only on dead organic matter are termed saprophytes ; those 
that develop in and at the expense of the living organism, para- 
sites. These latter by their growth cause certain pathologic con- 



196 



TEXT-BOOK OF PATHOLOGY. 



ditions in the host, and are called pathogenic. By obligate sapro- 
phytes or parasites Ave mean those that can exist only under the 
conditions named ; by facultative saprophytes and parasites, those 
that can develop under both conditions. 

Conditions of Growth. — Certain surrounding conditions 
are necessary to bacteria, and any marked change in them will 
inhibit the growth or totally destroy it. 

Mechanical Conditions. — A slight shaking of a liquid culture 
seems to help the development of bacteria, while a more violent 
and long-continued agitation, destroys them. 

Physical Conditions. — Electrical currents destroy the growth, 
but probably by the action of certain products of the electrolysis, 
and not by direct action. 

Light. — Diffused daylight inhibits the growth of bacteria : sun- 
light and, to a less extent, electric light destroy them. 

Heat. — A certain temperature is necessary, the degree varying 
with the species of microbe. Most of the water bacteria and sapro- 
phytes grow between 0° and 30° C. (32° and 86° F.), the optimum 
being 15°-20° C. (59°-68° F.) (Psychrophilic). The pathogenic 
nourish between 10° and 45° C. (50°-113° R), best at the 
body-temperature, 37° (98.6° F.) (Mesophilic). There are some 
that develop well at 40°-70° C. (i04°-158° F.) (Thermophilic). 
Above these limits the members of the several groups are killed, 
and each bacterium has its own thermic death-point. That of 
most of the pathogenic varieties lies between 50° and 60° C. 
(122° and 140° F.). Below the lower limit the growth is in- 
hibited only; very low temperatures ( — 250° C. ; — 418° F.) hav- 
ing been used without preventing the future development of the 
microbe. 

Spores are extremely resistant to higher temperatures. While 
no bacterium can live after exposure to 100° C. (212° F.), the 
spores of some of the earth microbes are killed only after exposure 
for an hour to steam heated to 115° C. (239° F.)/ 

Chemical Conditions. — The essential substances for the growth 
of bacteria are water, carbon, nitrogen and oxygen, and certain 
salts. For the carbon, they require already prepared carbon com- 
pounds, as the sugars, glucose, saccharose, lactose, etc., mannite, 
glycerin — in fact, most of such as are soluble in water. Most of 
the proteids and many simpler substances, even such as ammonium 
carbonate, furnish the nitrogen. Free oxygen is necessary for 
many microbes. Those for which this is absolutely required are 
termed obligate aerobic. Facultative aerobes are those that grow 
best in the presence of oxygen, but may develop in its absence. 
Anaerobic microbes are those that grow best without oxygen and 
are also obligate and facultative. It has been found possible to 
produce races which, although naturally obligate anaerobic^ 
develop also in an atmosphere of oxygen. 



BACTERIA AND DISEASES DUE TO BACTERIA. 



197 



Artificial Cultivation. — It is difficult and often impossible 
to study the growth of bacteria in their natural habitat. Hence 
we have recourse to artificial media, upon which we can study the 
growth and morphology of the organisms and the various phe- 
nomena that it brings about in different substances. 

Media for Cultivation. — Uschinsky's fluid is a non-albuminous 
medium : 



Water 1000 cc. 

Glycerin 30-40 gm. 

Sodium chlorid 5-7 gm. 

Calcium chlorid 0.1 gm. 

Magnesium sulphate . . ....... . 0.2-0.4 gm. 

Calcium phosphate 2.5-3 gm. 

Ammonium lactate 6-7 gm. 

Sodium asparaginate 3-4 gm. 



Bouillon. — Water, 1000 cc. ; lean beef or veal, 500 gm. ; salt, 
10 gm. ; peptone, 5 gm. The beef is soaked in water and then 
filtered. To the filtrate are added the salt and peptone, and the 
whole boiled for some fifteen to twenty minutes. It is then 
rendered slightly alkaline and filtered and sterilized. Ordinary 
beef-extract may be substituted for the fresh meat. Growths of 
bacteria in this medium are not especially characteristic, but in 
some species important differences appear. The liquid may become 
clouded or remain clear, the growth settling to the bottom of the 
tube as a flocculent deposit. The presence or absence of any 
growth on the surface of the bouillon (a membrane or mycoderm) 
is noted, as is also any change in the reaction. 

Peptone solution, prepared in the same way, but omitting the 
beef, is of use in the determination of the indol-reaction (see 
Bacillus typhi abdominalis). 

Liquid blood-serum is rarely employed. 

Milk, slightly alkaline and to which a small quantity of litmus 
or lacmoid may be added, is employed in determining changes of 
reaction and the action of caseating ferments. 

Extracts of many vegetable substances are also used, as hay, 
potato, brewer's malt, etc. 

Potato-extract, prepared by rubbing up 500 gm. of potato in 
500 cc. of water, decanting and diluting to 1000 cc, and adding 
40 cc. of glycerin, is a good culture for the Bacillus tuberculosis. 

Solid media. — The two most important solid media are gelatin 
and agar-agar. These are used in 10 per cent, and 1 per cent, 
solutions, respectively, in bouillon. Many bacteria produce a pro- 
teolytic ferment that liquefies gelatin. Other distinctions also are 
met with in cultures upon this media. 

Blood-serum is placed in test-tubes, slanted and sterilized for 



198 



TEXT-BOOK OF PATHOLOGY. 



one to two hours on five consecutive days at 60° C. (140° F.). 
The temperature is then raised to the point of coagulation of the 
albumin and the serum is thus solidified. Loffler mixes Avith the 
liquid serum one-third part of bouillon containing 1 per cent, of 
glucose. A more rapid way is carefully to solidify the serum on a 
water-bath or in the hot-air sterilizer, and then sterilize in steam 
on three separate days. 

Glucose, lactose, or saccharose, added to these media, may be 
used to study the action of the various ferments. 

Glycerin (5-6 per cent.) added to agar-agar forms good media 
for the growth of the tubercle-bacillus. 

Potatoes and other vegetables, cut in the form of half cylin- 
ders, are also used. 

Inoculation of Media. — In studying the growth of micro- 
organisms a portion of the culture-fluid, or other substance to be 
examined, is transferred to the various culture-tubes. To do this 
an inoculating-needle (dse) is employed. This is most conveniently 
made with a piece of platinum wire one to one and a half inches in 
length, either straight or with looped end, and fastened into the 
extremity of a glass rod. It should be an invariable rule to 
sterilize this needle in the naked flame both before and after it is 
used. In inoculating liquid media the transference of a loopful 
of the culture or other substance is made to the culture-tube. 
When solid media are employed a straight puncture may be 
made into the medium, or this latter may be solidified in a 
slanted position and the needle drawn along the surface. Due 
regard must be had for the richness in bacteria of the substance 
examined. With pure cultures but a minute quantity is trans- 
ferred ; with blood, however, large amounts, even \ to 1 cc, is 
often used. 

To study the appearance of the separate colonies cultures on 
gelatin or agar plates are made. The medium is melted and then 
cooled to a temperature not destructive to the bacteria ; 40° C. 
(104° F.) for agar, lower for gelatin. The liquid medium is in- 
oculated carefully and poured into sterilized shallow glass dishes. 
Those devised by Petri are useful. They are from three and a 
half to four inches in diameter and half an inch or less deep. 
Each microbe is supposed to form by its growth a separate 
colony, and in this Avay different species can be easily isolated 
and reinoculated on fresh tubes. When cultures are used, or 
when the bacteria are very numerous, the requisite dilution may 
be made by inoculating a second tube from the first, and in like 
manner a third from the second. Esmarch, instead of pouring 
plates, quickly rolled the tubes on a piece of ice or in ice-water, 
thereby forming a thin coating of the solid medium on the inner 
surface of the tube. If it is necessary to make a numerical esti- 
mation of the bacteria, definite quantities of the medium and 



BACTERIA AND DISEASES DUE TO BACTERIA. 199 



culture must be employed in the dilution. Sterilized pipettes 
are used in the process of diluting. 

Anaerobic Cultures. — These are made by growing the inocu- 
lated tubes or plates in the absence of oxygen, either by exhaust- 
ing the air or by replacing it by some inert gas, preferably 
hydrogen. Many tubes have been especially devised for this 
purpose. A more convenient method is to make a deep puncture 
in a gelatin or agar tube, and then preventing the absorption of oxy- 
gen by nearly filling the tube with melted sterile medium. It has 
been also proposed to inoculate the surface of such a tube with a 
culture of a strict aerobic microbe. Glass tubes of small caliber 
and a foot or more in length, and filled with inoculated melted 
media and sealed in a flame, give good results. 

Aerobic cultures grown in the absence of oxygen do not form 
spores, and may be destroyed by a subsequent temperature of 80° 
C. (176° F.), thus permitting the sporogenous anaerobic forms to 
develop in pure culture. 

FUNCTIONS AND PRODUCTS OF BACTERIA. 

The study of the substances that result from the action of the 
life of bacteria and the changes that they produce in their various 
media of growth is really a branch of organic chemistry. The 
function of bacteria is essentially a destructive one. They split 
up the higher nitrogenous and non-nitrogenous compounds into 
simpler substances. 

The various substances that are found in the media of bacterial 
growth comprise : (1) the components of the bacterial cell proper, 
as the proteins ; (2) the secretions of the cell, as the ferments ; 
and (3) substances that are the result of the action of microbes 
upon the medium of growth. 

(1) The first group has already been spoken of (see page 186). 
The proteins may produce suppuration (pyogenic) or fever 

(pyrogenic), or they may be the cause of an inflammatory process 
(phlogogenic). The best known examples are mallein, derived 
from the bacillus of glanders, and tuberculin, from that of tuber- 
culosis. These are pyrogenic when injected into animals suffering 
respectively from glanders or tuberculosis, but have no, or at least 
very slight, effect upon healthy subjects. Other proteins are shown 
to have similar effects on tuberculous animals. In practice the 
curative effect of these has not proved of much worth. 

(2) The second group of products includes the ferments and 
possibly the toxins. 

Ferments. — A ferment is a complex body about which we 
know but little except the effects that it produces. By its pres- 
ence, and probably without entering into intimate chemical com- 
bination, it possesses the power of breaking up more highly organ- 



200 



TEXT-BOOK OF PATHOLOGY. 



ized nitrogenous and non-nitrogenous compounds into simple, 
and more diffusible molecules. They are termed enzymes or un- 
formed ferments in contradistinction to the bacteria themselves, 
which are called formed or living ferments. That the action of fer- 
ments is not due directly to the microbe is shown by the facts that 
bactericidal substances, such as phenol (5 per cent.), chloroform, 
ether, etc., have no effect on them, and that cultures freed from 
bacteria by filtration still possess fermentative power. The 
action of ferments is termed fermentation, but the term is more 
especially limited to their effect upon non-nitrogenous compounds, 
particularly the carbohydrates. The result of fermentation upon 
nitrogenous material is called putrefaction, which generally occurs 
with, though often without, the formation of odorous gases and 
other substances. 

The principal bacterial ferments are : 

Proteolytic Ferments. — These transform albumins into more 
soluble and diffusible substances. One form very often met with 
is that which liquefies gelatin. This acts in an alkaline medium, 
and is therefore akin to the animal ferment trypsin. This lique- 
faction of the gelatin affords a means of distinguishing many species 
of microbes. 

Diastatic Ferments. — These transform the starches into sugars, 
and are found in many bacterial cultures, as of Bacillus mallei, 
Bacillus pneumoniae, etc. 

Inverting Ferments. — These change the non-fermentiscible su- 
gars into those that undergo direct fermentation. Such ferments 
are found, for instance, in cultures of Spirillum cholera? and 
Metschnikowi. 

Emulsifying Ferment. — This is formed by but few microbes. 
One example is Micrococcus pyogenes tenuis. 

Coagulating Ferment. — One of the means of differentiation of 
bacteria is the coagulation of milk used as a culture-medium for 
the bacteria under observation. This coagulation is due not to 
acidity produced in the medium, but to the action of a ferment. 

Some varieties of microbes produce a ferment that has the 
power of dissolving this coagulum when formed (casease) ; and 
still others produce both ferments — the coagulating and the dis- 
solving. 

Hydrolytic ferments are such as break up urea into ammonium 
carbonate and hippuric acid into glycocol and benzoic acid. 

Fat-splitting ferments split the fats into glycerin and the fatty 
acids. 

Oxidizing and nitrifying ferments are other less important 
forms. 

Effects of Ferments. — The single or combined action of 
these various ferments causes certain special kinds of fermentation 
distinguished by the principal substance produced. Alcoholic, 



BACTERIA AND DISEASES DUE TO BACTERIA. 



201 



lactic-acid, and butyric-acid fermentation of the sugars, acetic- 
acid fermentation of alcohol (Bacillus acidi lactici, Bacillus butyri- 
cus, Bacillus acidi butyrici, Bacillus aceticus, etc.) ; cellulose fer- 
mentation with the production of carbonic-acid gas and ammonia ; 
nitrification, due to the oxidation of ammonium and the production 
of nitrates (Winogradsky's nitromonas) and nitrites ; mucoid fer- 
mentation of glucose and invert-sugar are examples. 

(3) Substances produced by bacteria from the culture-media 
and tissues are varied and numerous. Besides those produced by 
the various fermentative processes there are : the products of 
digestion of albumin, alburnoses, peptone, etc. ; the ptomains ; ni- 
trogenous substances, as leucin and tyrosin, methyl-, dimethyl-, 
trimethyl-, ethyl-, propylamins ; organic fatty acids, formic, acetic, 
propionic, butyric, margaric, lactic, etc. ; certain aromatic com- 
pounds, as indol, phenol, kresol, skatol, mercaptan, hydrocbinon, 
etc.; and finally, hydrogen, carbonic dioxid, hydrogen sulphid, 
-ammonium, water, etc. 

Toxins. — Further, the pathogenic bacteria produce both by 
analysis and synthesis certain toxic substances which are akin to 
the poisonous venom of certain serpents and other animals, and to 
-certain poisonous principles of plants, as abrin and ricin. These 
are of indefinitely determined character, and act deleteriously upon 
the organism only after the lapse of a certain time — a period of 
incubation. They are considered the specific toxins of the several 
bacteria. According to some, these give all the reactions of 
albumin, and have been termed toxalbumins (Brieger). It is 
probable, however, that a toxalbumin is but an impure form of 
the true toxin, a combination of it and various substances derived 
from the medium of growth. Some authors regard it as an albu- 
minose ; others, as a peptone. Most recent investigators look 
upon the toxin as a ferment akin to the diastatic or hydrolytic 
ferments. Roux and Yersin, in their monograph on the Bacillus 
diphtheria?, hold this view. Many facts seem to support this 
theory. The analogous pathologic action of the toxins and fer- 
ments, their common origin, their destruction (oxidation) in the 
presence of light, their precipitation by alcohol, their precipita- 
tion from solutions by colloid bodies, their long and imperfect 
dialysis, all point to this. High temperatures affect both simi- 
larly, both being destroyed at from 60° to 100° C. (140° to 
212° F.). Chemical substances that have no effect (chloro- 
form, ether, etc.) on the ferments are without action upon the 
toxins ; and, vice versa, those that destroy the ferments (for- 
maldehyd) are also injurious to toxins. Both may be absorbed 
with impunity through the intestines, although pathogenic when 
injected subcutaneously or intraperitoneally. When the microbe 
is grown in some inorganic medium, or in a non-albuminous 
one (as Uschinky's solution), the toxic principle obtained 



202 



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corresponds in its chemical reactions to a ferment. Most import- 
ant is the fact that extremely minute doses are effective. Fer- 
ments act without regard to the mass employed, and it would 
seem that toxins act in almost imponderable amounts. It has 
been estimated that T qVo g m - °f tetanus toxin will kill a horse 
weighing 600 kg. — six hundred million times its weight ; and 
that u m g- °f tuberculin causes a reaction in a diseased man 
weighing 60 kg. — sixty trillion times its weight. Finally, both 
act only after a definite period of incubation. Courmont and 
Doyon found that by increasing the amounts of tetanus toxin 
injected into a dog they were not able to diminish beyond a defi- 
nite limit this latent period. Blood taken from the animal during 
the subsequent convulsions caused, when injected into another 
animal, an immediate tetanic attack. According to these authors, 
the ferment, possibly not toxic in itself, is capable of elaborating 
within the body or culture-medium the tetanizing substance. 

Considerable light has been thrown upon the nature of toxins by 
the recent investigation of Ehrlich and others who have followed 
him. These investigations have been mainly concerned with the 
behavior of the toxin toward the antitoxin bodies. Ehrlich has 
found that the serum contains at least three distinct substances : 
the toxin proper, toxoid, and toxone. The toxin is the active 
poisonous element; but, aside from its toxic property, it has a dis- 
tinct combining ability, so that it enters into combination with 
antitoxin. A given serum, however, will combine with a greater 
quantity of antitoxin than the toxic power of the serum would 
indicate. In other words, there are other combining bodies which 
have no toxic power. A serum as it grows older loses in toxic 
power without losing in combining power. This is due to the 
conversion of toxin into toxoid. The toxone has similarly the 
combining power for antitoxin, but is slightly toxic, being capa- 
ble, in the case of diphtheritic serum, for example, of producing 
the post-diphtheritic paralyses. It is, however, not a derivative 
of the toxin, but results from a direct action of the bacterium, 
and is produced simultaneously with the toxin. The dissocia- 
tion of combining power and toxic power is explained upon the 
assumption that each molecule of toxin contains a combining sub- 
stance or group and a toxic group. To the former the name 
haptophore group and to the latter the term toxophore group has 
been given. The probable nature of these will be referred to in 
the discussion of Ehrlich's theory of immunity. 

Fate of Toxins. — It is certain that there exist in various cells 
of the animal organism certain oxidizing ferments by which the 
toxin is destroyed. Not all of the toxin is thus oxidized. A part 
is eliminated unchanged through the kidneys in the urine and to- 
some extent through the liver in the biliary secretion. Beside 
these there is still another method of defence of the organism 
against the action of toxin — the antitoxin (q. 



BACTERIA AND DISEASES DUE TO BACTERIA. 203 



Chromogenesis. — Many bacteria form colors which give to 
the culture a characteristic appearance. Some attempt has been 
made to classify those pigments according to their solubility in 
alcohol, ether, etc. The pigment-forming bacteria themselves are 
called chromophoric when the pigment is a component of the bac- 
terial cell itself ; ehromoparie, when the coloring-matter is an 
excretion and the microbe remains colorless; and paraohromo- 
phoric when both conditions exist. The production of the pig- 
ment depends to some extent upon the constitution of the medium, 
and it is possible to produce cultures and even races of pigment- 
forming bacteria by the use of appropriate media. 

Photogenesis. — The phenomenon of phosphorescence ob- 
served in decaying fish is due to the action of bacteria. This 
production of light is observed in many of the cholera-group of 
vibriones. 

THE LOCAL EFFECTS OF BACTERIA. 

These may be either (a) mechanical or (b) histologic, the me- 
chanical effects being least in importance, (a) Sometimes masses 
of micro-organisms more or less completely occlude small blood- 
vessels and occasion secondary changes in the tissues in this 
mechanical way. In other cases the obstruction is incomplete, 
but occasions thrombosis in the blood-vessel and various conse- 
quential disorders, (b) The histologic changes occasioned by 
bacteria are proliferative and destructive, among the latter being 
various degenerations and necrosis. The proliferative changes 
may be non-specific or specific — that is, there may be simply 
proliferation such as occurs from any irritation ; or there may be 
special forms of proliferation more or less characteristic in extent, 
distribution, and nature of the individual micro-organism. This 
is seen in the characteristic lesions of tuberculosis, glanders, 
rhinoscleroma, etc. The cellular degenerations and necroses occur 
coincidentally or subsequent to the proliferative changes. On the 
contrary, in many cases the first effects of bacterial invasion seem 
to be degeneration or necrosis of the tissues immediately around 
the organisms. 

EFFECT OF TOXIC PRODUCTS OF BACTERIA. 
• 

Bacteria usually gain entrance into the animal body through 
some lesion of the epithelial layer, often the result of traumatism. 
Sometimes the microbes find in certain cavities of the body favor- 
able conditions for growth, as in the pulmonary or alimentary 
tracts, and there develop and elaborate their toxins. 

Intoxication and Infection. — In one class of diseases the 
infecting microbe remains localized at the point of inoculation, and 



204 



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is never or only exceptionally found in the fluids of the body, the 
general symptoms of the disease being due to absorption of the 
toxic products. Such are true Intoxications. In other cases the 
microbe is found circulating in the blood throughout the body 
and finds lodgement in most of the organs. These are called In- 
fections. Tetanus is the type of the first class ; anthrax, of the 
second. There is, however, no distinct line to be drawn, for the 
symptoms of ail infections are due to the toxins and other toxic 
products. While some bacteria always produce pure intoxications 
(tetanus), most of them may, under varying conditions, cause 
either intoxications or infections. This difference is due to a 
relative lack of virulence. Either the microbe is weak in toxin- 
producing power or the resistance of the tissue too great. The 
toxin is essentially negatively chemotactic (see Inflammation), and 
thus prevents the phagocytic action of the leukocytes ; while 
many other bacterial products and the bacterial proteins (Bnchner) 
are positively chemotactic. When a pathogenic microbe is want- 
ing in virulence, there is a determination of leukocytes to the 
point of inoculation and Suppuration results. A virulent microbe 
in the strict sense, then, is one that easily invades the animal body 
and there produces its more or less powerful toxin ; an avirulent 
one produces but little, if any, toxin and is destroyed by phago- 
cytosis, either with or without suppuration. 

Sapremia, Septicemia, and Pyemia. — From local sup- 
purative foci toxic products may be absorbed into the general 
circulation, and a condition known as Sapremia results. The 
infecting bacterium itself may invade the blood-current without 
giving rise to any secondary collection of pus. This is termed 
Septicemia. When, however, the microbe is carried to various 
parts of the body and there gives rise to secondary suppuration, 
the condition is called Pyemia. 

The destruction of leukocytes that takes place in the formation 
of pus is due probably to bacterial proteins. From this point of 
view suppuration is not specific, and its production by various 
chemical substances proves this. 

IMMUNITY. 

Definition. — In the present state of our knowledge of the 
condition of immunity it is most difficult to give a precise defini- 
tion of this term. It denotes that condition of an organism which 
enables it to resist the attacks of bacteria and their toxic secre- 
tions. In one sense it is the reverse of susceptibility. An animal 
that is not susceptible to an infection is said to be immune, and 
the term immunization is applied to the process by which an 
animal becomes thus refractory. 

Varieties. — Immunity may exist in an animal naturallv as 



BACTERIA AND DISEASES DUE TO BACTERIA. 



205 



an inheritance from immune ancestors (Natural Immunity). While 
absolute immunity is rare, examples of relative immunity are com- 
mon. It may be individual or racial. Thus dogs and Alge- 
rian sheep are refractive to anthrax, while other species of sheep 
are extremely susceptible to this infection. The lower animals in 
general seem to be perfectly immune to certain diseases common 
to man, such as syphilis. Immunity may be produced by a 
previous infection (Natural Acquired Immunity), or by arti- 
ficial means (Artificial Acquired Immunity). It may be the result 
of injections of cultures of the specific microbes, the virulence of 
which has been naturally or artificially reduced, as in the vaccines 
of variola and anthrax ; or of cultures, the living organisms hav- 
ing been destroyed by heat or other means ; or of filtered cultures, 
as in the production of diphtheria-serum ; or of the serum of ani- 
mals that have been rendered immune by these methods. In the 
first three cases the condition is more lasting and seems to be a 
permanent adaptation of the organism (Active Immunity)', while in 
the last case it is but temporary (Passive Immunity). 

In many cases immunity asserts itself against both the infect- 
ing microbe and its specific toxin, as in the rat with regard to the 
diphtheria-bacillus and its toxin ; but more often an animal is 
resistant to the infection, though susceptible to the toxin. An 
example of this is the action of the guinea-pig toward tetanus 
(Vaillard). The reverse may be true, and we see an injection of 
tuberculin without effect upon a healthy animal that is very 
susceptible to tuberculous infection. Most commonly natural 
immunity exists toward the infecting microbe and not its toxin. 

Mechanism of Immunity. — In many cases the fluids of 
the animal organism prevent the growth (inhibitory action), or 
wholly destroy the bacteria (bactericidal action). Thus the blood 
of the naturally immune rat is bactericidal to the anthrax bacillus. 
Very many examples of this coexistence of immunity and bacteri- 
cidal power of the blood can be given, and some authorities suppose 
this to be the general explanation of the mechanism of immunity. 
According to Buchner, this action is due to the presence in the 
blood and fluids of the body of certain albuminous bodies, which 
he terms Alexins. These are probably leukocytic in origin, and 
are not specific in their action, but protective toward all micro- 
organisms. This coexistence of bactericidal action and immunity, 
however, is by no means universal. Rabbits, for instance, possess 
a bactericidal blood-serum, but are not naturally immune to 
anthrax ; while, on the contrary, the adult dog is immune to this 
disease, though its serum has no effect upon the Bacillus anthracis. 

Another theory asserts that the inhibitory effect of the serum 
causes some change in the vital properties of the bacteria. Cul- 
tures of bacteria in the serum from immune animals seem to show 
some such effect, but this is probably due rather to the immuniz- 



206 



TEXT-BOOK OF PATHOLOGY. 



ing action of the serum in which they are suspended, as bacteria 
freed from this by nitration may show no such physiologic 
degeneration. 

A theory of great importance is that of Phagocytosis of Metsch- 
nikow. He holds that the destruction of the microbes in the 
animal body is to be explained, not by the conditions of the body- 
fluids, but by purely cellular activity. The infecting microbes 
are taken up by certain cells of the organism and are destroyed 
by intracellular digestion. These cells — phagocytes — are of two 
kinds : the mobile macrophages, including the mononuclear and 
polymorphonuclear leukocytes ; and the fixed macrophages, in- 
cluding the vascular endothelial cells, the cells of the bone-marrow 
and spleen, certain connective-tissue cells and Kupfer's cells, and 
even those of the nerve- and muscle-tissue, xlfter injection of a 
culture into the subcutaneous tissue of an animal naturally or arti- 
ficially immune, he noticed that the bacteria were all taken up by 
the leukocytes. That these microbes were still living and viru- 
lent, and were not taken up as mere dead matter, Metschnikow 
regards as fully established. One proof he cites is the fact that 
an exudate containing no free bacteria, but all intracellular, is 
capable of producing cultures on artificial media and causing in- 
fection in susceptible animals. 

To these facts Pfeiffer opposes the experiment of injecting 
cholera vibriones into the peritoneum of artificially immune guinea- 
pigs. He observed a complete destruction of the microbe by the 
peritoneal fluid — an agglutination into masses and a gradual de- 
generation. There were few, if any, leukocytes present, and he 
therefore claimed that such destruction was entirely extracellular 
and humoral in character. This property of destroying or dis- 
solving bacteria has been termed the " lysogenic" action of serum. 
However, if a preliminary injection of some substance that deter- 
mines a local leukocytosis is made, there occurs, instead of the 
reaction of Pfeiffer, a true phagocytosis. Metschnikow interprets 
Pfeiffer's phenomenon as the result of a dissolution of the leukocytes 
by bacterial action, and solution in the peritoneal fluid of the de- 
structive substances. It " is not a general phenomenon, and 
occurs only after intraperitoneal injections, and then only incon- 
stantly." 

Recent investigations by Gruber, Dunham, Widal, and others 
have shown that the serum of animals or man rendered immune 
(naturally or experimentally) to infection with the bacilli of 
typhoid fever, cholera, the bacillus coli, etc., causes agglutination 
and flocculent precipitation of the respective bacteria from their 
bouillon cultures. (For further details see Typhoid Fever.) 
This phenomenon (reaction of Gruber- Widal) has been interpreted 
as representing the mode of defence of the organism against in- 
fection, and the reaction has therefore been considered as one of 



BACTERIA AND DISEASES DUE TO BACTERIA. 207 



immunity. Many facts, however, militate against this view, and 
make it seem at least equally probable that it is a reaction of in- 
fection rather than of immunity. 

Authors quite generally agree that the bactericidal substances 
are derived from the leukocytes : one school, however, holding 
that phagocytosis is but a secondary and infrequent phenomenon ; 
the other, that it is the fundamental principle of immunity. 

Whether or not phagocytosis is an essential element in immu- 
nity, many points have been established by corroborative investi- 
gations. It is certain that phagocytosis does occur after subcuta- 
neous injection ; that this is much more marked in resistant and 
immune animals than in susceptible ones ; that such intraphago- 
cytic bacteria, at least in the early stages of the process, are still 
living and virulent ; and that the same phenomenon takes place 
even in the peritoneum after a preliminary injection of a positively 
chemotactie substance. Metschnikow has attempted to prove that 
phagocytosis may be exhibited toward fluid poisons as well as to 
particulate substances; but this view has been practically dis- 
proved by Ehrlich. 

Toxin-immunity ; Antitoxin. — Immunity is manifested in two 
ways: against the microbe, or -against the toxin; and the sub- 
stances that so act are therefore anti-infectious or antitoxic. One 
theory explains the condition of immunity by supposing that the 
cells of the body become accustomed to the poison (the old theory 
of Chauveau). A blood-serum, however, may be extremely anti- 
infectious without having any antitoxic properties, and numerous 
examples of this prove that the theory just mentioned cannot be a 
sufficient explanation. 

The term antitoxin is applied to a substance or substances in 
the serum of an animal that protects against a specific disease ; 
the serum is generally both antitoxic and anti-infectious. The 
two best known examples are the tetanus and diphtheria antitoxins, 
although in the laboratory antitoxic serum has been prepared for 
many of the infections of man and of the lower animals. 

Toxin-immunity exists naturally in some individuals against 
certain animal poisons, such as the poisons of snakes, scorpions, 
etc., and chemical poisons and alkaloids, as arsenic, abrin, ricin, 
etc. It may also be developed by frequent exposure to such 
poisons. Similarly, immunity against the toxin of a bacterium is 
produced by the injection of gradually increasing doses of the 
microbe and its products. Either a culture which has been steril- 
ized by filtration or by heat, or one containing bacteria of very low 
virulence, is used for the first injection. Preferably, small doses 
of the toxin freed from microbes by filtration are used. The doses 
are then increased until the animal is able to react against a small 
injection of the pure culture, and this is then given in increasing 
quantities. An animal thus treated is often able to withstand tre- 



208 



TEXT-BOOK OF PATHOLOGY. 



mendously large doses of culture. Curious and at present unex- 
plainable conditions often arise. For instance, the antitoxin may 
disappear from the blood of an animal thus artificially immunized 
without any loss of immunity, and some animals die from the dis- 
ease whose blood is still extremely antitoxic, a condition, as it is 
called, of supersusceptibility. These few facts seem to point out that 
immunity cannot be due to the antitoxic action of blood-serum. 

Formerly Behring explained all toxin-immunity as a histogen- 
ous immunity : that is, that the tissues of the body become accus- 
tomed to the toxin, a sort of Mithridatization. Later, however, 
he regarded acquired immunity, both active and passive, as an 
hematogenous immunity and due to the action of an antitoxin. 

Antitoxin was formerly regarded by many as a modification 
of the toxin by cellular action ; more recently it has been shown 
to be a substance elaborated by the cells under the stimulation of 
the toxin. 

Electrical Production. — Some investigators believed it possible 
to produce antitoxin in vitro by the action of either the continuous 
current or the rapidly interrupted direct current on the toxin. If 
this is so, the fact would point toward a direct modification. In 
the light of recent knowledge it seems likely that a toxin of 
lesser virulence, and not an antitoxin, was produced. This less 
virulent toxin might prove useful in developing immunity, just as 
non-virulent cultures do, and thus it seemed as if an antitoxin had 
been produced by the electric current. 

Action of the Antitoxin. — It was at first thought that the reaction 
between toxin and antitoxin was a purely chemical one, but prob- 
ably, as in bacterial immunity, it is an indirect one. A mixture of 
snake-toxin and its antitoxin which has no effect when injected into 
an animal, if previously heated to 70° C. (158° F.), may cause the 
death of the animal. It is supposed that the antitoxin is destroyed 
at that temperature, while the toxin is not. The death of super- 
susceptible animals cannot be due to any lack of antitoxin, but 
may be explained by a want of reaction of the body-cells. 

On the other hand, however, there are many experiments that 
seem to show the reverse ; that the neutralization may take place 
in the test-tube, and that it is really a chemical and not a physio- 
logic reaction. 

Among the protective substances described are the defensive 
proteids of Hankin or the alexins of Biichner. The former 
further subdivides them into sozins — those proteids present in the 
normal animal body — and the phylaxins — those in the body of the 
immune animal. The former are bactericidal and globulicidal, 
destroying the red and w T hite blood-corpuscles, and are easily 
destroyed by light and a temperature of 55° C. (131° F.). The 
phylaxins, the true antitoxins, are neither bactericidal nor globu- 
licidal, and withstand a temperature of from 70° to 80° C. (158° 



BACTERIA AND DISEASES DUE TO BACTERIA. 209 



to 176° F.). In their other chemical reactions they are similar 
to the toxins. 

Hankin further divides the sozins and phylaxins, according to 
whether they act against the microbe itself or its toxin, into myco- 
and toxo-sozins and myco- and toxo-phylaxins. 

There is a certain amount of immunity that can be produced 
by the injection of substances that have an attractive power for 
microbes (positive chemotaxis), such as salt-solution, peptone, ex- 
tracts of certain organs. 

This immunity, however, is not specific, but acts toward all 
varieties of bacteria. It is found that even the so-called specific 
antitoxins are active against other kinds of toxins, as tetanus-anti- 
toxin is partially preventive against snake-poison. It is therefore 
difficult to draw a distinct line between the specific and non-specific 
forms of antitoxin. Indeed, it is questionable if our present 
knowledge on the whole subject is sufficient to allow us to formu- 
late a definite theory of immunity. 

Ehrlich's Side-chain Theory of Immunity. — The recent theory 
elaborated by Ehrlich, and designated Seitenketten Theorie, explains 
the phenomena of immunity better than any other hitherto pro- 
posed. In the first place, the toxin, according to this theory, has 
a twofold nature and composition, one element representing the 
poisonous action, the other the combining power. The former, 
which might be considered as residing in special groups of the 
molecule, he termed the toxophore group ; the latter, the hapto- 
phore group. The toxophore group may readily become weaker, 
with no alteration in the haptophore group. This is seen in the 
transformation of toxin into toxoid (see Toxin). When a poison 
of any sort is introduced into the body, it fixes itself upon certain 
cells or upon cells in general through the junction of the hapto- 
phore group with somewhat similar groups contained in the fixed 
cells. The poison thus anchored is in position to attack the cell 
through the activity of its toxophore group. The combining por- 
tions of the cell are likened to the side chains of organic chemical 
bodies, as, for example, the lateral chains of benzol. They are 
independent of the central core or central group of the cell which 
is concerned in the proper functional activity. When a toxin has 
combined with the cells through the activity of the side chains 
of the latter, a destruction of the side chains ensues, and, if the 
toxophore group is active, a greater or less destruction of the cell. 
As a consequence of this destruction, and in the same manner as 
proliferation of fixed tissues follows the destruction of parenchyma, 
new formation of side chains occurs. This, like the products of 
the connective tissues after the destruction of parenchyma, is apt 
to be excessive, and the side chains are broken from the parent 
cell and carried into the circulation, where they constitute anti- 
toxin. They exist in the serum in solution, and the lysogenic 

14 



210 



TEXT-BOOK OF PATHOLOGY. 



power of the serum or of the plasma is probably concerned in this 
solution. The original side chain attached to the parent cell is 
not antitoxin ; rather, the reverse. It serves to attach the toxin 
to the cell, which is thus exposed to the toxophore. When the 
side chain is liberated and dissolved in the blood-plasma, it is an 
antitoxin, for it fixes the toxin and prevents the latter from 
reaching the vulnerable cell. If the antitoxin is thus the deriva- 
tive of normal cells and a constituent of normal cells, it seems 
likely that it might be abstracted from such cells in other ways 
than through the action of toxin ; and this has been accomplished. 
The toxin of tetanus fixes itself upon the nerve-cells promptly, 
and it has been found that emulsions of normal brain-tissue have 
antitoxic properties. 

Elimination. — Antitoxin is probably eliminated through all of 
the secretory organs. It has been found in the urine and to a 
large extent in the milk. Brieger and Ehrlich obtained a quite 
concentrated form of antitoxin by precipitation of the casein by 
ammonium sulphate and purification by dialysis. As in the case 
of toxins, the whole of the antitoxin seems to be carried down by 
the precipitated colloid casein. 

DISEASES DUE TO BACTERIA. 

The bacterial diseases form a large and increasing group. In 
some cases it has been shown by the positive application of Koch's 
rules (see page 31) that the suspected micro-organisms are the 
actual causes of the diseases under consideration ; in more numer- 
ous instances all of the rules cannot be applied, but other consid- 
erations go far toward establishing the specific nature of certain 
bacteria ; in still other cases the evidence warrants a strong suspi- 
cion of the pathogenicity of bacteria found in connection with cer- 
tain diseases, but there is nothing approaching actual demonstration. 

Division of infectious diseases into those of certain and those 
of uncertain bacteriology must cause differences of opinion. It is 
adopted only for convenience, the merits of each individual case 
being considered in the discussion of the individual diseases. 

DISEASES OF CERTAIN BACTERIOLOGY. 

SUPPURATIVE DISEASES. 
Definition. — Under this heading we include for the present 
various forms of suppurative inflammation, such as furunculosis, 
abscess-formation, and allied diseases, like osteomyelitis, endocar- 
ditis, etc. 

Ktiology. — Numerous organisms have been found to have 
the power of producing suppuration. Among these the staphylo- 



BACTERIA AND DISEASES DUE TO BACTERIA. 211 



coccus group is most important. The Streptococcus pyogenes seu 
erysipelatis is also of great significance ; less frequently the Dip- 
lococcus pneumoniae, the Pneumobacillus of Friecllancler, the Ba- 
cillus pyocyaneus, the typhoid bacillus, the Bacillus coli communis 
or the Bacillus pyogenes fcetidus, the gonococcus, and others. 
Some cases are due to a single organism ; in many there is double 
infection. 

1. The Staphylococcus Group. — Among these have been de- 
scribed three important forms, the Staphylococcus pyogenes 
aureus, albus, and citreus. 

The Staphylococcus pyogenes aureus is a minute, rounded 
body about t 5 q- to 1 [i in diameter, having no motility and not 
forming spores. When found in the tissues the cocci are apt to 
be associated in clusters, whence the term staphylococcus (Fig. 79). 




Fig. 79.— Staphylococcus pyogenes albus (Jakob). 



Sometimes they are grouped in pairs, and may thus present a re- 
semblance to gonococci. The opposed surfaces, however, are flat 
instead of concave, as is the case with the gonococci. The 
staphylococcus may be stained with ordinary anilin solutions and 
is beautifully demonstrated by Gram's method. Cultures are 
easily obtained upon the ordinary media. The most characteristic 
growth is that upon agar. Along the line of inoculation a moist 
colony develops, with at first a whitish but soon an orange-yellow 
color. The growth in gelatin causes rapid liquefaction and the 
precipitation of orange-yellow particles. The growth is best ob- 
tained at oven-temperatures, but may be secured at lower degrees. 

Distribution. — The Staphylococcus aureus is frequently found 
upon the skin or in the various external secretions of healthy in- 
dividuals. It does not seem to flourish anywhere apart from the 
bodies of man or animals, but may remain in an active state in the 
dust of rooms or upon clothing and the like. It has been found 
in various lesions of the bodv ; notably, however, in furuncles, ab- 



212 



TEXT-BOOK OF PATHOLOGY. 



scesses, and carbuncles, and in ulcerative conditions of the exterior 
or of the mucous membranes. It is also frequent in internal suppu- 
rative inflammations, such as malignant endocarditis, osteomyelitis, 
appendiceal abscesses, etc. In many of these lesions other organ- 
isms may be associated. 

Pathogenicity. — When pure cultures are injected into animals 
abscesses are produced and a fatal termination may follow. In 
the latter cases diffusion through the blood is found, and infarcts 
of the kidneys, lungs and other organs caused by bacterial emboli 
are discovered. Multiple abscesses may be seen. The organism 
readily loses its virulence, as in the case of those found, upon the 
skin of healthy persons, and in other accidental situations. When 
rubbed in a virulent state into the skin of man it produces ab- 
scesses or boils. 

Staphylococcus Pyogenes Albus. — This organism is practi- 
cally identical with the last-named in morphology, but in culture 
produces a white instead of a yellow growth. It has been found 
as a frequent harmless parasite of the skin (Staphylococcus epiderm- 
idis albus of Welch). It occurs in abscesses and various suppu- 
rative diseases, but rarely alone. As a rule, it is associated with 
the golden staphylococcus or other organisms. It is distinctly less 
virulent than the aureus. 

Staphylococcus Pyogenes Citreus. — This form is the least 
important of the three. It is not so common and, as a rule, less 
virulent. It differs in the brilliant lemon color obtained upon 
culture in various media. 

2. The Streptococcus Pyogenes seu Erysipelatis. — The Streptococ- 
cus pyogenes was first studied by Rosenbach in cases of suppuration. 
A similar organism was afterward described as the Streptococcus 
erysipelatis by Fehleisen. It would seem, however, that these 
two organisms are identical. At all events, there are no distin- 
guishing features which we can point out. The streptococcus is a 
small spherical organism of variable size, frequently associated in 
chains of from three to twenty or more individuals (Fig. 80). It 
is easily stained with ordinary anilin solution or by Gram's 
method. The cocci are not motile. Spore-formation has not 
been observed, but occasionally in chains one of the individual 
members is larger than the rest, suggesting arthrospores. Upon 
artificial media scanty but rather characteristic growths are ob- 
tained. On the gelatin plate there are formed small, translucent, 
whitish or yellowish colonies of irregular outline. The gelatin is 
not liquefied. Upon agar a very thin, transparent growth forms 
around the line of inoculation. It consists of separate colonies 
which do not become confluent. 

The distribution of the streptococcus is much the same as that 
of the staphylococci, though it is less commonly discovered about 



BACTERIA AND DISEASES DUE TO BACTERIA. 213 



the healthy body. It may, however, be found upon the mu- 
cous membranes or in the various secretions or excretions of the 
body. It is probably a strict parasite, multiplying only within 
the living organism. 

In disease it has been found in various forms of suppuration, 
such as phlegmonous forms of inflammation of the subcutaneous 
or submucous tissues, either alone or in association with other 
organisms. It occurs occasionally in focal suppurations, such as 
abscesses, though these are more commonly due to staphylococci 
alone. The streptococcus occurs at times in ulcerative endocarditis, 
and not rarely in infectious endometritis. Streptococcic inflam- 
mations of the throat are of great interest. They may occur in 
persons previously in good health, or in the course of infectious 
diseases, like scarlatina, measles, or influenza. To the clinician, 
the resulting lesion may be indistinguishable from that of diph- 
theria ; bacteriologic examination alone serves to establish the 




Fig. 80.— Streptococcus pyogenes (Jakob). 



diagnosis. The streptococcus is found in all cases of erysipelas, 
in the tissues, and in the serum or other exudations. 

Pathogenesis. — When cultures of streptococci derived from 
suppurative diseases or from erysipelas are injected into rabbits 
erysipelatous inflammation may result. Subcutaneous injections, 
however, may cause no local or general symptoms in mice or rab - 
bits. It Avould seem that animals are rather resistant. 

Pathologic Physiology. — When injected into the subcu- 
taneous tissue the staphylococcus produces local effects. The 
organism may become liberated, gain entrance to the circulation, 
and produce widespread results ; but it does not seem to produce 
toxins that cause generalized results. The effects of the staphylo- 
coccus seem to be due rather to a certain poisonous body con- 



214 



TEXT-BOOK OF PATHOLOGY. 



tained in the organism itself. This has been termed the bacterial 
protein, and it seems to belong to the group of alkaline albumin- 
ates. This body by its chemotactic effect causes the leukocytic 
accumulations found in suppurative inflammations. The same 
body, or perhaps others, appears to have a simultaneous irritative 
and stimulating influence upon the fixed connective tissue of the 
part, leading to proliferation. The staphylococcus also leads to 
liquefaction in the tissues, as in gelatin, but whether directly or 
through the accumulation of bodies derived from leukocytes is 
uncertain. The defence of the organism against the staphylococ- 
cus is partly mechanical and partly vital. The leukocytes prob- 
ably englobe a certain number of organisms and cause their 
destruction, while soluble bactericidal bodies, probably albumin- 
ous in character, seem to be produced in the course of the infec- 
tion. These have been termed alexins, and are largely derivatives 
of the leukocytes. 

The streptococcus would seem to be more active in the produc- 
tion of soluble toxins than the staphylococci. The toxin has been 
made by inoculating small quantities of bouillon with virulent 
cocci, allowing these to grow for several weeks, and then destroy- 
ing the organisms by heat. The injection of the toxins thus 
produced leads to local and general reaction. An antistreptococcic 
serum has also been produced, and seems to possess some power to 
combat infection with the organism in question. 

Other Organisms of Lesser Importance. 

The Bacillus pyocyaneus is an occasional pathogenic organism found in 
pus having a bluish or greenish color. The bacillus is small in size, fre- 
quently occurring in chain-formation, and is actively motile. 

Upon artificial media it produces colored growths and a soluble pig- 
ment, which gives to the culture-medium for some distance from the growth 
a greenish, or in some cases a dark-blue, coloration. The organism in 
pure culture is highly virulent, producing intense suppurative inflamma- 
tions. Occasional instances of general pyocyaneus infection have been 
observed. 

The Bacillus pyogenes foetidus is probably identical with the Bacillus coli 
communis, or is at least a close relative. These organisms, as well as the 
typhoid bacillus, the Diplococcus pneumoniae, the Diplococcus meningitidis, 
and the Pneumobacillus of Friedlander, are referred to elsewhere. 

Micrococcus Tttragenus. — This form is a micrococcus from 1 to 2 y in 
diameter, and receives its name from the peculiar association in groups of 
four. It occurs in the sputum and contents of cavities in pulmonary 
phthisis, and occasionally elsewhere. It may give rise to general sepsis. 

Bacillus Lactis Aerogenes. — This organism resembles Friedlander's pneu- 
mobacillus quite closely. In large doses it occasions suppuration in animal 
experiments, while in man it has been found associated with purulent 
cystitis, pyelitis, and pyelonephritis. In consequence of its fermentative 
power it may occasion pneumaturia. 



BACTERIA AND DISEASES DUE TO BACTERIA. 215 



GONORRHEA. 

Definition. — Gonorrhea is an infectious inflammation of the 
urethral or other mucous membranes due to a specific organism, 
the gonococcus of Neisser. 

Etiology. — There is no doubt that the gonococcus is the 
specific cause of gonorrhea. This organism is a micrococcus, 
usually arranged in pairs, the opposed surfaces of each being 
slightly concave. This arrangement has suggested the designa- 
tion " biscuit-shaped " diplococcus (Fig. 81). Sometimes groups 




Fig. 81.— Pus from gonorrhea, showing gonococci (Jakob). 

of four or more are found, while in other cases the cocci occur 
singly. The organisms are abundant in the pus of acute gonor- 
rhea, less abundant in advanced stages, in the pus of gonorrheal 
salpingitis or other conditions, and may not be discovered at all. 
They generally occupy the pus-cells, lying in the protoplasm, and 
occasionally within the nucleus, either in small numbers or so 
abundantly as to fill the cell uniformly. In the tissues the same 
intracellular position is usual, but here, as in the free pus, some 
organisms may generally be found between the cells. The gono- 
coccus stains readily with ordinary solutions of anilin dyes, but 
is readily decolorized by Gram's method. 

Cultivation of the gonococcus is difficult. Growths may, how- 
ever, be obtained at 37° C. upon media consisting of human blood- 
serum and agar-agar, upon acid gelatin or albuminous urine. The 
growth in blood-serum consists of small colonies of grayish color 
that coalesce and form a film on the surface of the medium ; around 
the colony may generally be seen an irregular and inconspicuous 
extension. 

The gonococcus cannot be positively distinguished by its 
morphology nor by the intracellular position. Other organisms 
may in certain stages of their growth show a typical biscuit-form 



216 



TEXT-BOOK OF PATHOLOGY. 



(staphylococci and others) ; and the intracellular position is not 
rarely assumed by a variety of bacteria. The failure to stain by 
Gram's method and the failure to grow on ordinary media are 
strong points in favor of the gonococcus. Typical cultures alone 
settle the diagnosis. 

Pathogenicity. — It has been demonstrated by direct implanta- 
tion of pure colonies upon the healthy urethra that this organism 
will cause characteristic gonorrhea. Urethritis may, however, be 
due to other organisms ; the specific form termed gonorrhea is 
probably always due to the gonococcus. Secondary lesions, such 
as salpingitis, oophoritis, arthritis, peritonitis, conjunctivitis, endo- 
carditis, etc., may also be due to this organism, no other form of 
bacteria being present. Sometimes, however, complications, such 
as periurethral abscesses, suppurative adenitis, etc., are due to 
secondary infections. 

Pathologic Anatomy. — The lesions of gonorrhea will be 
considered elsewhere. Suffice it to say in this place that the 
organism causes suppurative catarrh of the mucous surfaces with 
which it comes in contact. There is abundant round-cell infiltra- 
tion, and the organisms tend to penetrate deeply into tissues. 

Pathologic Physiology. — Gonorrhea is in most cases a 
purely local disease. Little is known of its power to produce 
soluble toxins. The distant lesions are in all cases, as far as we 
definitely know, dependent upon deposit of the specific organism. 
These have been found in the effusions of arthritis and in the 
vegetations of gonorrheal endocarditis, as well as in the blood in 
the last named condition. 

CROUPOUS PNEUMONIA. 

Definition. — There are a number of forms of inflammation 
of the pulmonary tissues to which the term pneumonia is appli- 
cable. The most definite form of disease is that spoken of as 
croupous, fibrinous, or lobar pneumonia. In its typical form this 
is a specific and well characterized disease. It is infectious, more 
or less contagious, and caused by a specific organism. 

Etiology. — The organism most likely the cause of croupous 
pneumonia is the Diplococcus pneumoniae. This organism is also 
called the pneumococcus and the pneumobacillus. In reality the 
last name is most applicable, but has not found general favor. 
The diplococcus of pneumonia Avas recognized in the saliva of 
healthy persons by Sternberg and Pasteur, but its relation to 
croupous pneumonia was demonstrated by Frankel, and later by 
Weichselbaum. The individual organism has a somewhat elon- 
gated, lanceolate shape, and therefore deserves the name bacillus, 
though it does not always show this bacillary shape distinctly 
(Fig. 82). In the sputum and lungs, and in the blood of inocu- 



BACTERIA AND DISEASES DUE TO BACTERIA. 217 



latecl animals, it is commonly found in pairs ; the broader end of 
the organisms adjacent, and the pointed ends projecting outward ; 




Fig. 82.— Diplococcus pneumoniae in the blood (Frankel and Pfeiffer). 

and the group is surrounded by a transparent capsule, which does 
not take stains and therefore becomes conspicuous (Fig. 83). 

Sometimes a number of the organisms are 
grouped in chains, so that the name Strep- 
tococcus pneumoniae has been suggested. 
The capsule is not seen when the organ- 
ism is obtained from cultures. The dip- 
lococcus does not possess individual motil- 
ity and has no flagella. It does not seem 
to produce spores. 

It may be readily demonstrated in the 
sputum or in the tissues by staining with 
the ordinary anilin dyes or by Gram's 
method. 

Cultivation. — The diplococcus grows 
readily upon ordinary media, excepting potato. It forms charac- 
teristic colonies upon agar-agar plates or in gelatin. Upon the 
surface of the agar there appear transparent drop-like colonies 
hardly visible to the naked eye, which under the microscope have 
a finely granular appearance. Upon gelatin plates similar growths 
are produced, while in gelatin punctures the growth occurs along 
the path of the wire as granular whitish spots separated from each 
other. The organism tends to die out very readily in cultures, 
and also loses its pathogenic property when propagated for several 
generations. It is most luxuriant at 37° C. (98.6° F.). 

Pathogenicity. — The specific character of this organ has not 
been definitely proved according to the rules of Koch, but it is 




Fig. 83.— Diplococcus pneu- 
moniae : a, cocci, without cap- 
sules ; b, single and paired 
-cocci, with capsules ; c, chain- 
form ; d, colony of cocci (Zieg- 
ler). 



218 



TEXT-BOOK OF PATHOLOGY. 



highly probable that it is the usual cause of pneumonia. The 
diplococcus is frequently found in the saliva of healthy persons. 
When this is introduced into animals, particularly rabbits, the 
animal dies, with evidences of rapid sepsis. The post-mortem 
shows some fibrinous exudate and occasionally a little pus at the 
point of inoculation. The spleen is enlarged, and capsulated bac- 
teria of distinct lanceolate form are widespread throughout the 
body. Injections of lung-tissue or of pneumonic sputum produce 
similar results, and the organism in pure culture likewise causes 
this form of septicemia. It has been claimed that inhalation or 
injection of the diplococci into the trachea will produce true pneu- 
monia in susceptible animals. This remains to be proved more 
definitely. 

Besides the diplococcus there are certainly other elements 
which contribute to the causation of the disease, else the frequent 
occurrence of the micro-organism in question in the saliva would 
make pneumonia a much more common affection. The nature of 
the contributing causes is, however, obscure. Exposure to cold, 
general depression of the system, traumatism, alcoholism, and other 
causes certainly predispose or help to determine the occurrence of 
the disease. These causes may act by temporarily increasing the 
virulence of the diplococcus or by lowering the resistive power. 

Certain irregular forms of lobar pneumonia may be caused by 
streptococci, staphylococci, the Bacillus pneumoniae of Fried- 
lander, the influenza bacillus, that of typhoid fever, etc.; but true 
croupous pneumonia is probably always due to the Diplococcus 
pneumoniae. 

Pathologic Anatomy. — (See Diseases of the Lungs.) 

Pathologic Physiology. — The diplococcus produces, in the 
first place, local lesions of the lungs ; and, in the second place, 
systemic intoxication by toxins of uncertain character. The 
organism itself, however, gains access to the blood and may pro- 
duce secondary lesions in other organs. Infection with the diplo- 
coccus of pneumonia causes a pronounced reaction on the part of 
the blood in the form of leukocytosis. This is not invariable, but 
is usually seen. After the attack of pneumonia there is temporary 
immunity, and it has been claimed that animals may be immun- 
ized for considerable lengths of time. This, however, is uncertain. 
No definite antitoxic substance has thus far been secured. 

The Diplococcus in Other Diseases. — The Diplococcus 
pneumoniae has been found in various conditions complicating 
pneumonia, and occasionally without the existence of a previous 
croupous pneumonia. Among other lesions, meningitis, pleurisy, 
and other inflammations of the serous surfaces, abscesses, otitis 
media, and arthritis have been found to be due to this organism ; 
or, at least, this organism alone has been found in some of these 
cases. 



BACTERIA AND DISEASES DUE TO BACTERIA. 219 




OTHER FORMS OF PNEUMONIA. 

Among other varieties of pneumonia may be mentioned the 
catarrhal or lobular form, the tuberculous form, and various irreg- 
ular pneumonias, partly cellular, partly fibrinous, partly purulent 
or hemorrhagic. A number of different organisms may be found 
in such cases, and some of these may be of etiologic importance 
in certain cases. 

The Bacillus Pneumoniae of Friedlander. — This organism was 
regarded at one time as the cause of croupous pneumonia. It is 
probably in most cases an accidental associate, though it may 
occasionally be the cause of catarrhal or irregular forms of pneu- 
monia. It occurs as a distinct bacillus, 
usually in pairs and surrounded by a cap- 
sule like that of the diplococcus (Fig. 84). 
Sometimes it may form chains of three, four, 
or more organisms. It stains well with the 
anilin dyes, but is decolorized by Gram's 
method. A characteristic culture is ob- 
F mo^^ a Fri 1 e , SaSde?." tamed in gelatin. The puncture-culture is 
characterized by a luxuriant growth at the 
top and a considerable vegetation all along the track. This leads 
to a nail-shaped growth. The gelatin does not liquefy. Upon 
agar a considerable whitish or yellowish growth occurs upon the 
surface. There is formation of gas in media containing glucose, 
and often also on potato. 

In catarrhal pneumonia this organism may be discovered, or 
the various forms of staphylococcus or the Streptococcus pyogenes ; 
more rarely the influenza-bacillus, the Bacillus coli communis, the 
typhoid bacillus, and others are discovered. In some of these 
cases the disease may be the result of double infection. 

Tubercular pneumonia, in which a uniform pneumonic process 
is found in the lungs, may be due to simple infection with the 
tubercle-bacillus, or to mixed infections. 

Irregular pneumonias may be of varying pathologic type, and 
may be occasioned by a great variety of organisms. No satis- 
factory classification can be attempted, as the limitations of the 
term pneumonia can scarcely be established. 



RHINOSCLEROMA. 

Rhinoscleroma is a disease affecting the skin about the anterior 
nares and adjacent parts, and probably caused by a specific bacil- 
lus. The disease has been especially observed in central Europe. 
It presents itself in the form of nodular thickening of the skin of 
the nose and lip, and sometimes spreads to the neighboring mu- 
cous membranes — mouth, pharynx, or larynx. In the latter situa- 



220 



TEXT-BOOK OF PATHOLOGY. 



tions ulceration of the surface is frequent ; the lesions of the skin 
rarely ulcerate. Histologically the growth consists of round 
granulation-tissue cells. Frequently the cells suffer hyaline de- 
generation, forming rounded hyaline bodies. The bacilli may be 
found between the cells and within these, especially such as pre- 
sent hyaline degeneration. The micro-organism resembles the 
bacillus of Friedlander, but, unlike this, stains well by Gram's 
method, and when cultivated upon blood-serum or agar retains its 
capsule. In other respects the two forms are identical. Inocu- 
lation-experiments have thus far failed to produce the disease in 
animals. 

DIPHTHERIA. 

Definition. — Diphtheria is an infectious and contagious dis- 
ease caused by a specific bacillus. 

Etiology. — The Bacillus diphtherias was discovered by Klebs, 
and more accurately studied by Loffler, and is therefore called the 
Klebs-Loffler bacillus. This organism is a rod about the length 
of the tubercle-bacillus and twice its thickness, with somewhat 
swollen ends. It is readily demonstrated in the local lesions of 
the mucous membranes or skin, where it may be quite abundant ; 
the individual bacilli, however, are separate from one another. 
The organism is peculiar in its great irregularity of shape and 



% 



3^ K 



V 



Fig. 85.— Bacillus diphtherise from a pure culture. 



size, particularly in cultures (Fig. 85). Branched forms have 
been observed, and some investigators view the organism as a 
streptothrix or even as one of the hyphomycetes. Frequently one 
end is especially large, giving a club-shaped appearance; some of 
the bacilli are very large ; some present rounded granules at 
either end, the so-called polar granules or Ernst bodies. The 
bacillus is readily stained with aqueous solutions of basic stains, 
especially with those rendered slightly alkaline. (Loffler's stain 
— saturated aqueous solution of methylene-blue, 30 cc, in aqueous 
solution of potassium hydrate, 1 : 10,000, 100 cc. — is the favorite 



BACTERIA AND DISEASES DUE TO BACTERIA. 221 



stain.) The stained specimen shows the morphology of the 
bacillus very clearly. The rounded ends generally stain more 
deeply than the shaft of the bacillus, so that the appearance some- 
what suggests a diplococcus. Not rarely transverse fractures give 
the organism the appearance of disjointed segments. There are 
no flagella, and the bacillus is not motile. Spores have not been 
demonstrated. 

Cultivation. — The most characteristic cultures are obtained 
upon blood-serum, especially such as contain a small amount of 
glucose. Upon this medium there is formed within six, twelve, or 
twenty-four hours a thin, whitish or yellowish-white layer of ir- 
regular outline, often showing separate smaller colonies around 
the edge. A small portion of the colony may be removed and 
stained, and the diagnosis thus established with ease in a short 
time. Other organisms found in the throat are slower in growth, 
and do not therefore interfere with the diagnosis. 

Pathogenicity. — When cultures in bouillon are injected beneath 
the skin of a guinea-pig a fibrinous inflammation with more or less 
Avidespread edema results, and the animal dies in from twenty-four 
to thirty-six hours. Necrotic foci in the liver and other organs 
are found post-mortem ; the neighboring lymphatic glands are 
enlarged. If the animal survive, paralysis may make its appear- 
ance, as in human beings recovering from the disease. 

Non-pathogenic diphtheria bacilli are found in the pharynx of 
healthy individuals in some cases, as well as upon the hands, hair, 
or other parts of the body. They are also found in various forms 
of rhinitis, conjunctivitis, and non-diphtheritic angina. These 
may differ from the virulent bacilli in being somewhat shorter 
and in growing more luxuriantly. Their distinctive character, 
however, is their harmlessness when injected into animals. The 
term jpseudodiphtheria bacillus is unfortunate, as it is prob- 
ably the same organism, but one having lost its virulence by 
growth in an unfavorable situation. Moreover, the name pseudo- 
diphtheria bacterium was formerly applied to various organisms 
having nothing whatever in common with the Klebs-Loffler 
bacillus. 

Neisser has devised a staining method that has some usefulness in 
distinguishing diphtheria bacilli from the pseudodiphtheria or xerosis 
bacilli: 

(1) Methylene-blue, 1 g. 
96 per cent, alcohol, 20 cc. 
Ac. acet. glac, 50 cc. 
Water, 950 cc. 

(2) Vesuvin, 2 g. 
Water, boiling, filter, 1000 cc. 

Cover-glass preparations are stained for from one to three seconds in 
solution 1, washed, and treated with solution 2 for from three to five seconds 
and washed. 



222 



TEXTBOOK OF PATHOLOGY. 



Cultures must be made on Loffler's blood-serum for at least nine hours, 
and not longer than twenty to twenty-four hours, at a temperature of 34°- 
35° C. (not over 36° C). This procedure, according to Neisser, brings out the 
Ernst granules in the true diphtheria bacillus, while the pseudo variety 
remain negative. Frankel holds that microbes that do not give the 
granules with this method are of the pseudo variety. 

Loftier and others hold that while this reaction is a useful addition to the 
differential diagnosis, it must not be relied upon absolutely. 

According to Neisser, a further aid in differentiation is obtained by 
making impression preparations from six-hour old serum-cultures. In these, 
true diphtheria bacilli will be found lying side by side or crossing each 
other, while the pseudodiphtheria bacilli and xerosis bacilli adhere so 
closely to the culture-medium that they are not removed with the cover- 
glass. 

Klebs-Loffler bacilli may be found in the pharynx of a person 
showing no indication of disease. This means that the organism 
has not found a favorable soil for its development or no abrasion 
or opening into tissues that will support its growth. The bacil- 
lus may, however, thrive and multiply for a considerable time 
upon the mucous membrane of such a throat, as it may upon food, 
clothing, or other infected materials. 

Predisposing Causes. — Some predisposition is necessary for the 
development of the disease. In part this is personal, some indi- 
viduals being highly susceptible, others scarcely at all. In part, 
accidental conditions, such as pharyngitis, laryngitis, abrasions, 
etc., furnish a favorable opportunity for the infection. 

The diphtheria of birds, calves, and certain other animals is 
distinct from the human disease ; and the organisms are in no 
way related. Human diphtheria may occur in cats, and these 
animals may propagate epidemics. 

Distribution of the Bacilli. — The organisms are abundant in the 
pseudomembranes of diphtheria, but are only exceptionally found 
in the blood or internal organs. The visceral or nerve-lesions are 
due to the toxins, and not to the bacillus. The same is true of 
experimental diphtheria. The internal lesions may be produced 
by injection of the toxin obtained by filtering a bouillon-culture 
through a Pasteur niter. 

Pathologic Anatomy. — Diphtheria is primarily a local dis- 
ease of the pharynx (pharyngeal), of the larynx (laryngeal), of 
the nose (nasal), or of the skin (dermal). The bacillus lodges in 
the mucous membrane or skin, and produces a pseudomembrane. 
This consists of fibrinous exudation in the form of fine granular 
material or a fibrillar network, in which are embedded the epi- 
thelial cells and other tissue-elements and infiltrating leukocytes. 
The epithelial cells rapidly undergo coagulation-necrosis or granu- 
lar degeneration, as do also the connective tissues when the pro- 
cess extends beneath the mucosa. The blood-vessels become 
obstructed by thrombosis or compression, and the tissue is there- 
fore avascular. Nearly always the pseudomembrane thus formed 
is attached to the underlying tissues, and when removed a raw 



BACTERIA AND DISEASES DUE TO BACTERIA. 



223 



and bleeding surface is exposed. The depth of involvement, 
however, varies ; sometimes the snbmucosa is soon involved ; 
more often the disease is practically confined to the mucosa. 

The macroscopic appearance is that of a whitish, dirty-yellow- 
ish, or brownish membrane upon the mucous lining of the throat. 
This begins as one or several patches upon the tonsil, and spreads 
rapidly to the neighboring parts. In other situations the appear- 
ance is much the same. Inflammatory swelling beneath and 
around the diseased area is habitual. It is of great clinical im- 
portance to recognize that true diphtheria may occur in the form 
of typical follicular tonsillitis. 

Internal or visceral lesions may occur in the course of diph- 
theria or during convalescence. They are due to the action of the 
toxin, and not of the bacillus. Necrotic foci in the liver, showing 
advanced cellular degeneration of the cells with hyperchromatosis 
of the nuclei, and similar lesions of other organs, may be seen in 
the human body, as in animals killed with the organism or its 
toxin. Myocarditis and myocardial degeneration, renal degenera- 
tion and nephritis, and, most interesting of all, degeneration of the 
peripheral nerves and neuritis, may be met with. All of these 
will be described elsewhere. 

Pathologic Physiology. — As has been said, the disease is 
primarily local, and the bacilli nearly always remain localized in 
the superficial lesions. The general manifestations — fever, pros- 
tration, and the visceral lesions — are caused by poisonous sub- 
stances elaborated by the growth of the bacilli. There are prob- 
ably several substances of this sort, but one in particular — the 
toxin — is most important. This may be obtained by filtering 
bouillon-cultures through porcelain, and by its injection the con- 
stitutional and some of the local manifestations of the disease may 
be induced in animals. Successive introduction of increasing 
doses of toxin causes the development of antitoxic substances that 
may finally accumulate in the blood to such extent that the ani- 
mal becomes immune to the most virulent bacilli. The antitoxic 
substance or substances, or antitoxin, found in the blood and the 
blood-serum of immunized animals, will render other animals im- 
mune for a time, or combat and overcome the disease if already 
existing. Simultaneous injection of antitoxin and of many times 
the ordinarily fatal dose of toxin or diphtheria-cultures leaves an 
animal unharmed. Later, when the immunity has passed olf, a 
small dose of toxin or culture without the antitoxin will kill the 
same animal. The value of the antitoxin in animal experimenta- 
tion is beyond doubt. In the human being there is scarcely any 
doubt of its potency, though, of course, crucial experiments cannot 
be made. 

After an attack of diphtheria there is temporary immunity, 
but this passes oif and successive attacks may thus occur in the 
same person. 



224 



TEXT-BOOK OF PATHOLOGY. 



TYPHOID FEVER. 

Definition. — Typhoid fever is an infectious disease, with 
characteristic lesions of the intestines, and due to a specific 
bacillus. 

Etiology. — Certain predisposing features make individuals 
more liable at one time than another to this disease. It occurs in 
adolescence and the young, though rarely also in the old. Cli- 
matic conditions are supposed to play some part, and doubtless do 
have an influence. Typhoid fever is especially a disease of the 
temperate zones, and is most abundant in the autumn. Drainage 
and other conditions affecting the surroundings of persons may 
influence the predisposition. One attack usually confers immunity 
for the rest of life ; exceptions, however, are met with. 

The Bacillus. — The Bacillus typhi abdomiualis, the specific 
organism, Avas discovered by Eberth and isolated by Gaffky. It 
is a short bacillus, from 1 to 4 p. in length and 0.5 to 0.8 fi in 
thickness. The ends are rounded and often somewhat plump. In 
culture these rods or bacilli occasionally form long chains, but in 
the tissues they are never so arranged. The organism is actively 
motile, this being due to flagella, of which there are eighteen or 
twenty attached to the periphery (Fig. 86). "When stained with 




Fig. 86— Bacillus typhi abdominalis, from an agar-agar culture six hours old, showing the 
flagella stained by Lomer's method ; X 1000 (Frankel and Pfeiffer). 

alkaline methvlene-blue or other stains there are sometimes seen 
dark-colored spots at the ends of the organism. These were 
formerly regarded as spores, but are now recognized as areas of 
condensation. Under certain circumstances the condensation is 
seen in the center and vacuole-like formations are found at the 



BACTERIA AND DISEASES DUE TO BACTERIA. 225 



ends. The organism is readily stained, but decolorizes very 
easily, and is therefore difficult to demonstrate in tissue. Pro- 
longed staining, however, and rapid decolorization sometimes give 
beautiful results. The bacilli are, as a rule, found in clusters. 
These groups may, however, be few in number, and thus difficult 
to detect in the organs. 

Cultivation. — Artificial cultures of the bacillus have been ob- 
tained from the spleen and other organs, as well as directly from the 
stools and urine of patients suffering from the disease. They grow 
very well upon the ordinary culture-media, such as agar-agar, gel- 
atin, and potato, the temperature of the body being most favorable, 
but some growth occurring at the ordinary temperature of the 
room. Upon gelatin and agar there are formed irregularly whitish 
films, which on close inspection with the lens show a granular 
appearance. This growth, however, is not distinctive. Upon acid 
potato a characteristic transparent pellicle is formed. This may 
be invisible except to the trained eye, but on scraping the surface 
with a platinum wire the pellicle can be raised, and on micro- 
scopic examination it is found to be composed of bacilli. Some- 
times the pellicle is yellowish or brownish. When cultivated in 
milk there is slight acidity, but coagulation does not occur. When 
grown in agar containing a little glucose practically no fermenta- 
tive gas results. Another feature of importance is the absence of 
indol-reaction, the addition of potassium nitrite and sulphuric acid 
to bouillon-cultures causing no rose color, such as occurs with 
some other organisms. 

Pathogenicity. — Animal-experimentation has thus far been un- 
satisfactory. A few observers have succeeded in producing intes- 
tinal lesions and illness by feeding animals with typhoid cultures, 
particularly after the stomach and intestines have been rendered 
alkaline with soda and peristalsis has been checked with opium. 
In most cases injection of the typhoid bacillus has produced sep- 
ticemic manifestations. The constant occurrence of the germ, its 
absence from other conditions, and the absence of any other germ 
as a constant accompaniment of typhoid fever, have led to the 
general acceptation of this as the specific cause. Moreover, its 
properties are such that the spread of the disease in the acknowl- 
edged ways is entirely compatible with the acceptance of the 
bacillus as the specific cause. 

The diagnostic features of the bacillus are plainly distinctive, 
except that the Bacillus coli communis has a puzzling resemblance. 
The latter, however, grows upon acid potato as a yellowish or 
brownish film, coagulates milk promptly and causes decided acid 
reaction, and is an active gas-producing organism when grown in 
glucose-agar. The serum-reaction of Wiclal is a recent and im- 
portant distinguishing mark. The serum from typhoid patients 
must not, however, be relied upon absolutely, as it may contain 



226 



TEXT-BOOK OF PATHOLOGY. 



substances produced by the Bacillus coli as well as those produced 
by the typhoid germ (see Widal reaction). 

Distribution. — The typhoid bacillus occurs both within and 
without the human body, and doubtless multiplies greatly in the 
external world when the conditions are favorable. It occurs in 
the lesions of the intestines and in the intestinal contents, espec- 
ially during the second and third weeks of the disease. It is 
usually less abundant, but often present in the spleen, liver, and 
kidneys ; it may occur in considerable abundance in these organs 
when there are local complications. It also occurs in the lungs, 
in the parotid gland, and in other organs, and post-typhoidal ab- 
scesses may contain the organism in abundance. Complicating 
lesions of other organs may be dependent solely upon the specific 
bacillus, this being capable even of acting as a pyogenic organism, 
or they may be dependent upon secondary or mixed infections. 
The bacillus is not found in the blood in abundance, but has been 
demonstrated in the blood derived from the macular spots in the 
skin. 

The typhoid bacillus is peculiarly resistant, and may thrive 
upon clothing, in soil, and in water for a long time. Cold has no 
effect, the germ being virulent after freezing and thawing several 
times. Carbolic acid in strengths that prove destructive to most 
organisms has little effect on this germ. These features explain 
the spread of the disease and its general prevalence. The organ- 
isms are discharged from the body of a patient suffering from the 
disease mainly in the stools, but in part also in the urine, sweat, 
and other excreta. If they are not at once destroyed, contami- 
nation of clothing, soil, water, etc. may occur, and subsequent 
infection of susceptible individuals takes place through drinking- 
water or food with which the infected water or other matters have 
come in contact. It is possible that infection may occasionally 
take place through the lungs by inhalation of dust. This must be 
very rare. Intra-uterine infection undoubtedly occurs in some 
instances in which the mother is suffering from typhoid fever. 

Pathologic Anatomy. — The lesions of typhoid fever are 
considered with the diseases of the intestines. It is important, 
however, to add in this place that widespread changes may occur 
in this disease as a result of the action of the bacillus, but especially 
of toxins. Thus there may be focal necroses in the spleen and 
liver, degenerative changes in the kidneys and muscles, and inflam- 
matory changes in various glandular organs, the periosteum, the 
bones, or the connective tissues, the result of the direct action of 
the bacillus. 

Sometimes typhoid infection occurs without specific lesions of 
the intestines, the disease in these cases presenting itself as a form 
of cryptogenetic sepsis. In cases of intra-uterine infection this 
form is habitual, intestinal lesions being exceptional. 



BACTERIA AND DISEASES DUE TO BACTERIA. 227 



Pathologic Physiology. — The typhoid bacillus produces 
by its local action toxic substances which give rise to fever and 
other general symptoms as well as to secondary lesions. Brieger 
and Frankel claim to have separated a specific toxalbumin. 
Whether this be the poison or not, there is no doubt that some 
form of toxin is present. During the existence of the disease the 
system reacts in some way as yet unknown to check its progress 
and to bring it to a termination at the end of four weeks, and 
permanent immunity is usually conferred. Whether or not there 
are distinct antitoxic substances remains to be determined. Pro- 
tective vaccination has been practised, but thus far no definite 
opinion as to its value can be formed. 

A reaction of importance is that studied by Gruber and per- 
fected by Widal. These observers showed that the serum of typhoid 
blood in certain dilutions causes the bacillus in culture to clump or 
form small masses and to lose its motility. If the serum be added 
to the bouillon-culture, the uniform turbidity of the latter is lost 
and the bacilli fall to the bottom as a sediment. Under the micro- 
scope the uniform distribution of the motile bacilli is destroyed, 
clumps being rapidly formed and the motility of the bacilli in the 
clumps rapidly or gradually subsiding. This reaction was found 
in 2283 cases of typhoid fever reported by various writers, and 
was absent in 109 cases of typhoid fever. It was absent in 
1365 non-typhoid cases, and present in 22 non-typhoid patients. 
It was therefore found in 95.5 per cent, of the typhoid cases, 
and was absent in 98.4 per cent, of the non-typhoid cases ; 
or, taking the entire 3779 cases, the correct result for diagnosis 
was arrived at in 96.5 per cent. The reaction sometimes persists 
for some years after the attack of typhoid fever. Sometimes it 
occurs in cases in which there is typhoid infection without typhoid 
fever in the ordinary sense. These facts may explain some of the 
positive results obtained in non-typhoid cases. The serum must 
be diluted with nineteen parts or more of water. Reactions with 
stronger serum or partial reactions may be deceptive. AVhether 
the Widal reaction is produced by a substance connected with the 
infection, or by substances concerned with immunization, is not as 
yet determined. 

BACILLUS COLI COMMUNIS. 

Synonyms. — Bacterium coli commune. A number of organ- 
isms described under different names are probably identical. 
Among these are Bacillus Neapolitanus of Emmerich ; Bacillus 
pyogenes foetidus of Passet. Several other organisms are either 
closely allied or identical. 

Morphology. — The Bacillus coli communis is an organism 
almost exactly like the typhoid bacillus in appearance. It is rod- 
shaped, but sometimes elongated and filamentous, at other times 



228 



TEXT-BOOK OF PATHOLOGY. 



(young forms) short and rather rounded — coccus-like. It is 
actively motile, and has flagella attached to the periphery of the 
bacillus. The flagella are less numerous than are those of Eberth's 
bacillus (three to ten), and the motility of the organism is less uni- 
form and active. It may be stained by ordinary solutions of anilin 
dyes, particularly with alkaline or carbolized solutions. It is de- 
colorized by Gram's staining-method. The stained bacillus shows 
light-colored or unstained portions like those of the typhoid bacil- 
lus. True spores have not been detected. 

Cultivation. — The organism grows luxuriantly upon ordinary 
media. The most distinctive growth is obtained upon acid potato. 
An elevated brownish colony is produced, which is usually easily 
distinguished from the typhoid culture in the same medium. 
When cultivated in gelatin or agar containing glucose active gas- 
production results. In liquid media (bouillon) a peculiar odor is 
developed. Addition of nitrites and pure hydrochloric or sulphuric 
acid causes a rose-red color — indol-reaction. 

Distribution and Pathogenicity. — The coli bacillus is a 
normal inhabitant of the gastro-intestinal tract. In certain in- 
flammatory diseases of the intestines, however, it seems to increase 
in numbers and doubtless also in virulence. The organism may 
be found outside the body in various situations, particularly in 
water. 

The bacillus coli is capable of producing inflammatory condi- 
tions in different situations. Injected into the peritoneal cavity 
of animals it gives rise to acute fibrinopurulent peritonitis, and in 
other parts of the body has analogous effects. 

It has been found in various diseases of the gastro-intestinal 
tract, of the biliary passages, of the urinary system, and of other 
parts, and is doubtless the direct cause of some of these, as the 
conditions present are practically the same as those produced by 
experimental inoculation of pure cultures. 

Among the gastro-intestinal troubles it has been found in sus- 
picious abundance in various forms of enteritis, in the distended 
and suppurating appendix, and even in Asiatic cholera. It is 
known that the strangulation of a knuckle of intestine by a liga- 
ture leads to rapid increase of virulence of the contained bacilli. 
It is possible that in appendicitis and in other intestinal diseases 
similar conditions lead to increased infectivity, and thus cause an 
ordinarily harmless organism to become virulent. In the cases of 
Asiatic cholera in which this organism has been found the specific 
germ of cholera has probably been overlooked or has disappeared 
during the rapid multiplication of the saprophytic Bacillus coli. 

Peritonitis may result from escape of the bacillus through a 
ruptured intestine or directly through the wall of the bowel. The 
latter is particularly prone to occur in cases of strangulation of the 
intestines. 



BACTERIA AND DISEASES DUE TO BACTERIA. 229 



Various inflammatory diseases of the urinary tract, such as 
cystitis, pyelitis, and pyelonephritis, seem to be occasioned by 
this same germ. 

Finally, there are cases of peritonitis secondary to enteritis, 
pleurisy, endocarditis, and other inflammatory diseases, apparently 
caused by this organism. 

Pathologic Physiology. — Little is known of the toxic 
effects of coli-infection. Some toxic substance is doubtless 
produced. A reaction similar to the Widal reaction obtained 
with the typhoid germ has been found to occur when 
cultures of the coli bacillus are subjected to the action of serum 
from an animal inoculated with this organism or from a person 
suffering with appendicitis or other diseases, either due to coli- 
infection or accompanied by such. Occasionally the coli bacilli 

>^yr^ 
1 *»- '/ f ;s"M i% 



"4.: 



Fig. 87— Spirillum of Asiatic cholera, from a bouillon-culture three weeks old, showing 
numbers of long spirals ; X 1000 (Frankel and Pfeiffer). 

agglutinate and their motility is checked by typhoid serum. The 
explanation of this may be that in certain cases of typhoid fever 
the coli bacillus is also active in the intestines, and in conse- 
quence a mixed form of infection is present. 

CHOLERA. 

Definition. — Cholera is an acute infectious and contagious 
disease caused by a spirillum or vibrio. 

Etiology. — the specific cause of cholera is the Spirillum or 
Vibrio cholerse Asiatics. This organism is frequently spoken of 
as the comma-bacillus of Koch. It is a, short rod, from 0.8 to 
2 fi in length, and usually somewhat curved. The term comma- 



230 



TEXT-BOOK OF PATHOLOGY. 



bacillus is applied to it on account of the latter fact. It is found 
abundantly in the rice-water discharges of choleraic patients, and 
is not rarely arranged in rows, though the vibriones are not actu- 
ally attached to one another (Fig. 87). It is motile, the motility 
being due to a single flagellum attached at one end. In artificial 
cultures the organisms are actually joined to form spirals of greater 
or less length, and these may present a rapid rotary movement. 

The demonstration of the cholera-spirillum is usually easy, as 
ordinary stains color it intensely. Even the flagellum may be 
stained by the ordinary stains, though more definitely shown by 
special methods. 

Cultivation. — The cultivation of the spirillum is usually easy. 

Cultures may be obtained upon agar-agar, blood- 
serum, or other media, but the gelatin-culture is 
most characteristic. In puncture-cultures the 
growth occurs along the entire length of the 
puncture, but particularly at the top, where the 
supply of oxygen is abundant ; and the gelatin 
becomes liquefied. This give rise to a peculiar 
nail-shaped or funnel-shaped formation (Fig. 88). 
In plate-cultures the growths first appear in the 
lower strata of the gelatin as small granular whit- 
ish spots which extend toward the surface, liquefy 
the gelatin, and thus produce excavations. The 
appearance to the naked eye suggests small air- 
bubbles in the media. Under low powers of the 
microscope the culture is seen to be coarsely 
granular, the size of the granules varying with 
the age of the culture. The bottom of the growth 
presents an appearance like that of a surface 
sprinkled with powdered glass. 

When grown in bouillon or other liquid media 
the cholera-microbe produces nitrites and inclol, 
so that the addition of a little pure sulphuric acid or hydrochloric 
acid leads to a reddish coloration. This may be extracted with 
chloroform or benzol, and " cholera-red " may be thus obtained. 

The cultures of cholera grow best at a temperature about that 
of the body, but they may thrive at much lower degrees of heat. 
Exposure to a temperature of 52° C. (125.6° F.) for four minutes 
may cause their destruction, but ten or fifteen minutes' exposure 
at 55° C. (131° F.) does not always prove destructive. They 
may thrive in distilled water, or in water containing saline 
matter ; in or upon various forms of food ; upon clothing and the 
like. The resistance, however, is not very great, and this has 
been urged as an objection to the likelihood of the organism being 
the cause of a disease having such evident tenacity. 

Pathogenicity. — The pathogenicity of the cholera-spirillum is 




Fig. 88.— Punct- 
ure-culture in gel- 
atin of spirillum of 
cholera; sixty hours 
old (Shakespeare). 



BACTERIA AND DISEASES DUE TO BACTERIA. 231 



now admitted universally. Injected into the peritoneum of ani- 
mals it causes a rapid fall of temperature, abdominal tenderness, 
and collapse. The peritoneum shows signs of beginning inflam- 
mation, and the organisms are found in abundance within the 
cavity. It has been possible also to produce intestinal changes 
almost, if not, identical with those of human cholera in animals by 
arresting the peristalsis of the intestines with injections of opium, 
rendering the liquids of the stomach alkaline with sodium carbonate, 
and then feeding cultures. In man a few auto-infections have 
been practised, the experimenter swallowing cholera-cultures. In 
one case at least typical cholera Avas admitted by Pettenkofer, the 
most important opponent of the acceptance of this germ as the 
specific cause. 

Other Causes Operating in Cholera. — Certain climatic conditions 
favor the development of the disease. Thus it is constant in cer- 
tain regions of India, and spreads thence when the conditions 
become favorable. The evidence shows that the germ is carried 
by individuals, or by infected food and the like. The disease 
flourishes in warm seasons of the year, and an epidemic is usually 
brought to a close by winter frosts. 

Individual disposition plays a part in the occurrence of the 
disease, for the germ is easily destroyed by the acid gastric secre- 
tions, and infection is therefore most likely to occur when gastro- 
intestinal derangements furnish a favorable predisposition. 

Pathologic Anatomy. — The lesions of this disease are 
found in the intestinal tract, and will be described in the appro- 
priate section. 

Secondary lesions of other organs are met with in severer 
cases, and result from the circulation of toxic substances produced 
by the bacillus. 

Pathologic Physiology. — A number of toxins have been 
isolated from the blood of cholera-patients and from cultures. 
The exact nature of these and the relations of the several forms 
remain to be determined. It is certain, however, that toxins pro- 
duced in the intestinal tract give rise to many of the symptoms 
of the disease. The human or animal organism in some way de- 
velops immunizing or protective substances in the course of infec- 
tion, and it has been found possible by a process of vaccination 
with cultures of gradually increasing virulence to protect animals 
and human beings from the disease. Pfeiffer found that the serum 
of animals so vaccinated had a distinct action upon cholera-spirilla, 
causing their agglutination or destruction, and probably in this way 
exercising a protective influence. This, or a similar, reaction has 
now been perfected in the case of typhoid bacilli, and forms the 
basis of the well-known Widal test. The same test is applicable 
to Asiatic cholera. The rapid and copious intestinal discharges of 
cholera lead to considerable inspissation of the blood, and doubtless 



232 



TEXT-BOOK OF PATHOLOGY. 



contribute to the causing of some of the symptoms of the disease. 
Examination of the blood during the height of the malady may 
show greatly increased numbers of red blood-corpuscles. 

Organisms Resembling the Cholera=vibrio. 

Spirillum of Finkler and Prior. — This organism was discovered 
by the investigators, whose names it bears, in the stools of a case 
of cholera nostras. It resembles the vibrio of Asiatic cholera in 
its shape and somewhat in its manner of growth and its produc- 
tion of the indol-reaction. It differs, however, in being somewhat 
longer and more slender and in coagulating milk when this is used 
as the culture-medium. The growth upon gelatin is more rapid, 
so that within twenty-four hours in the case of a puncture-culture 
the liquefaction has proceeded so far all along the puncture that an 
elongated sac-like excavation is formed, in which turbid liquid is 
contained. It has not yet been proved that this organism has an 
etiologic relation to cholera nostras ; its pathogenicity is im- 
probable. 

Spirillum Tyrogenicum. — This is an organism discovered in old 
cheese by Denecke. It resembles the last-named variety very 
closely, and differs from the vibrio of cholera in liquefying gelatin 
quickly, though the rapidity is not so great as in the case of the 
Finkler and Prior organism. 

Spirillum Metschnikowi. — This organism was discovered by 
Gamaleia in the intestines of chickens affected with choleriform 
disease. It is somewhat shorter and thicker than the cholera- 
spirillum. In culture it resembles the vibrio of cholera very 
closely, though the trained bacteriologist can easily distinguish 
them. The organism is non-pathogenic for man, but chickens, 
pigeons, and guinea-pigs are highly susceptible. 

Besides these spirilla or vibriones which have been discovered 
in various diseases, a number of organisms that resemble closely 
the spirillum of cholera have been found in the water of streams 
supplying the drinking-water of cities. Among these Neisser 
described the Spirillum Berolinensis, obtained from the water of 
the Spree in 1893. Dunbar and Oergel isolated a similar organ- 
ism from the water of the Elbe, and a number of others of like 
character are known. The relations, however, of the different 
forms to each other and the differentiation of these varieties have 
not as yet been definitely determined. 

Pathogenicity. — Some of the forms described produce violent 
gastro-intestinal disturbance and death in a certain proportion of 
animals prepared by injection of opium and alkalinization of the 
intestinal tract with soda and then fed with pure cultures of the 
organisms. They are evidently highly irritating bacteria, and 



BACTERIA AND DISEASES DUE TO BACTERIA. 233 

some remote relationship seems to exist between them. This, 
however, cannot be positively asserted. 



TUBERCULOSIS. 

Definition.— The term tuberculosis refers to various condi- 
tions due to infection with the tubercle-bacillus, no matter what 
the form or individual peculiarities of the case. The name was 
originally employed because of the occurrence of small nodules 
or " tubercles." It must be remembered, however, that other 
diseases show small miliary nodules, perhaps indistinguishable to 
the naked eye from miliary tubercles, and that tuberculosis some- 
times occurs without a single tubercle. 

Etiology. — Tuberculosis is infectious and contagious, the ba- 
cilli being transferred by the secretions and excretions from dis- 
eased persons to a susceptible individual through the air, food, 
drink, or in other ways. The infectious character of the disease 
was long suspected, but was definitely proved by Villemin in 
1865, and in 1880 Koch succeeded in isolating the infective ba- 
cillus. Predisposing causes are of some importance. Formerly 
family susceptibility was thought an all-important cause, and the 
disease was supposed to be transmitted directly in families. At 
the present time we recognize the transmission of susceptibility, 
and very rarely transmission of the disease itself, from parent to 
child. Susceptible persons frequently show delicate organization 
with poor development of the body, particularly of the chest. 
Besides inherited susceptibility, acquired predisposition may result 
from occupations which lower vitality, from grief, prolonged ner- 
vous strain and exhaustion ; and some one of the organs may be 
specially predisposed by injuries, as in cases of tuberculosis occur- 
ring in the lungs of those inhaling sharp particles of metal, coal, 
and the like. Such mechanical lesions prepare a place of lesser 
resistance, and tubercle-bacilli more easily gain a footing than in 
normal tissues. Continued local anemia seems to predispose. 

The tubercle-bacillus is a rod-shaped organism about 1.5 to 3.5 p. 
in length and from 0.2 to 0.5 fi in breadth. It often occurs in 
pairs or in groups, arranged end to end, but not rarely overlapping 
somewhat, and evidently not closely attached one to the other. 
A beaded appearance is caused by the alternation of portions 
well stained and intervening parts with little or no stain (Fig. 
89). These light areas were formerly regarded as spores (Koch), 
but are now believed to be the result of fragmentation of the 
bacillus and retraction of the substance of the organism, causing 
vacant areas. In other words, they are phenomena of degenera- 
tion. They are almost certainly not spores. The tubercle-bacillus 



234 



TEXT-BOOK OF PATHOLOGY. 



is not motile arid does not have flagella. It is therefore trans- 
ported by outside agencies entirely. Sometimes the organism 
presents itself in apparently branched forms. 

Artificial culture of the Bacillus tuberculosis was first success- 
fully accomplished by the use of blood-serum as a medium. 
The bacillus grows very slowly ; after ten days or two weeks 
the surface of the medium shows dry flakish deposits, somewhat 
resembling the scales in certain skin-diseases (Fig. 90). The 
edges of these flakes tend to elevate themselves a little, and the 
substance of the growth has a crumbled appearance. Placed under 
a cover-glass in mass and examined with the microscope these flakes 
are found to be composed of contorted masses of bacilli (Fig. 91). 
Pure cultures are best obtained from the lymphatic glands of ani- 
mals artificially infected and destroyed before the tuberculous 
foci have advanced to the stage of necrotic change. Cultures 
may be obtained with some difficulty from the sputum or other 



Fig. 89. — Tubercle-bacilli in the sputum; Zeiss's homog. immersion T V, Oc. 4; magnified 

about 1000 diam. 

excreta. At the present time blood-serum is less frequently used, 
as it has been found that agar-agar slightly acidulated and con- 
taining a large proportion of glycerin, and bouillon containing gly- 
cerin, serve as useful media. Even potato and other simple sub- 
stances are found to be satisfactory media. The bacillus requires a 
rather even temperature for its growth ; it flourishes best at 37.5° 
C. (99.5° F.), and does not grow below 29° C. (84° F.), or above 
42° C. (107.6° F.). Exposure to higher temperatures (75° C.) 
(167° F.) rapidly destroys it ; and strong sunlight is destructive. 
It requires considerable air and always grows upon the surface of 
the medium in which it is cultivated. Prolonged cultivation upon 
artificial media lessens its virulence. 

Demonstration. — The demonstration of the tubercle-bacillus by 
staining-methods is extremely easy and satisfactory. It has been 
found that this organism, like that of lepra and the smegma-bacil- 
lus, does not readily stain, but after receiving a stain retains it 
despite the action of strong mineral acids. Upon this principle 



BACTERIA AND DISEASES DUE TO BACTERIA. 235 



the methods of staining are based. Koch used as a stain a gentian- 
violet solution containing anilin-oil, the latter playing the part of 
a mordant or an agent to fix the stain in resistant bacilli. The 
specimen was then decolorized by treating 
it with a solution of a mineral acid, which 
removes the stain from everything but 
the tubercle-bacillus. A counter-stain 
mi^ht then be used to render the detec- 
tion of the bacilli more easy. 

The most convenient method 
following : sputum is spread 



m 



the 
film 





Fig. 90.— Culture of tubercle- Fig. 91.— Bacillus tuberculosis : adhesive cover- 

bacilli on glyeerin-agar. four glass preparation from a fourteen-day-old blood- 
weeks old (Frankel and Pfeiffer). serum culture: X 100 (Frankel and Pfeiffer). 



upon thin cover-glasses or slides. These are allowed to dry 
in air and then thoroughly fixed by drawing the specimen 
through a Bunsen flame three times ; a drop or two of Ziehl's 
solution of carbol-fuchsin (see p. 194) are added and heated 
until the liquid steams. After two or three minutes the stain is 
washed off with water and a few drops of Gabbett's solution 
(rnethylene-blue, 2 ; sulphuric acid, 25 ; water, 75) placed upon it 
and allowed to remain a minute or two. The specimen is again 
washed with water, and should then be uniformly blue ; if not, a 
little more Gabbett's solution is added as before. In this method 
the carbol-fuchsin stains everything, including the tubercle-bacil- 
lus ; the sulphuric acid of the second solution decolorizes every- 
thing but the tubercle-bacillus ; and the methylene-blue at once 
stains the cells and other elements, leaving the bacilli dark red. 
Even more satisfactory results may be obtained by allowing the 



236 



TEXT-BOOK OF PATHOLOGY. 



carbol-fuchsin to stain at ordinary temperatures for twelve hours ; 
and in the staining of bacilli in tissues this prolonged cold staining 
is particularly desirable. Gram's method gives positive results. 

Distribution of the Tubercle-bacillus. — This organism is prob- 
ably a pure parasite, occurring and multiplying only in the body 
or excreta of diseased individuals, human or animal. Sputa or 
other excreta containing the bacillus may dry and retain the 
bacillus in a dormant though still potential form for long periods 
of time, outside the body. Multiplication of the organism, how- 
ever, probably very rarely occurs, except within the body. The 
bacillus is found in the lesions of all parts of the body. 

Modes of Infection. — The bacillus may gain access to the body 
either by direct inoculation, by the inhalation or swallowing of 
the germs, or by intra -uterine transference through the placenta. 
Direct inoculation through external wounds is perhaps more fre- 
quent than is believed. Definite lesions of the skin have been 
caused by vaccination, and are not infrequent upon the hands of 
anatomists, in the form of the so-called anatomic tubercles. In 
some of the cases of scrofulous or tuberculous glands of the 
neck in children, it is likely that the bacillus gains entrance 
through abrasions of the skin or of the mucous membrane of the 
mouth or pharynx. Genital tuberculosis is quite possibly fre- 
quently produced by direct implantation. The most common 
form of infection is through the inspired air. The breath of 
phthisical patients does not ordinarily contain bacilli, but the dust 
of rooms in which tuberculous patients have lived may contain 
numerous bacilli in a dry state, and these readily become mixed 
with the air and are thus inhaled. Tuberculosis of the lungs, or 
more rarely of other parts of the respiratory tract, is thus produced 
in susceptible persons. The swallowing of tuberculous material 
may lead to tuberculosis of any part of the gastrointestinal tract 
by the direct inoculation that results. Thus intestinal tuberculosis 
in particular is produced. Sometimes, however, the bacilli pass 
through the wall of the intestine and cause a primary lesion in the 
lymphatic glands of the abdomen. The bacilli are swallowed 
with milk or meat, or they may gain access to the mouth, in the 
form of dust or particles of various kinds, and be swallowed with 
the saliva. The milk and meat of infected cattle frequently con- 
tain bacilli, and undoubted instances of infection in this way have 
been proved. The intra-uterine transmission of tuberculosis is 
rare, but does occur. Most of the cases, however, of tuberculosis 
in early life may be explained as post-natal infections through 
milk, inspired air, etc. 

Relations of Human to Animal Tuberculosis. — The lower ani- 
mals are liable to tuberculosis in varying degrees. The disease is 
very common among cattle and less frequent in hogs, goats, 
horses, dogs, cats, sheep, rats, guinea-pigs, and rabbits. Animals 



BACTERIA AND DISEASES DUE TO BACTERIA. 237 



become more susceptible when kept in confinement. Captive 
monkeys are particularly liable. Birds and fowl of various 
kinds are susceptible, though the disease is somewhat different 
in them from that seen in man. Recently tuberculosis of cold- 
blooded animals has been recognized. 

Animals may become infected from man, and may further 
spread the infection by their discharges or excretions. In the case 
of cattle the danger of dissemination is particularly great, as 
tainted milk is liable to produce intestinal tuberculosis, and meat 
if insufficiently cooked may similarly cause infection. 

Pathologic Anatomy. — Tuberculosis is characterized by the 
eruption of small nodules varying in size from one or two milli- 
meters in diameter to that of a small pea. These are known 
as miliary tubercles. As already mentioned, the latter in gross 
appearance are not distinctive of tuberculosis, as similar nodules 
are met with in other diseases. Besides the tubercle there are 
inflammatory lesions occurring between the tubercles and varying 
with the anatomic character of the organs affected. Thus in the 
lungs the tubercle may be inconspicuous, w T hereas the pneumonic 
infiltration of the lung-tissue surrounding the tubercles and filling 
in the spaces between them gives the organ its most striking 
anatomic characters. There are instances of tuberculosis in which 
the whole process runs its course without the development of any 
definite tubercles. For example, in the lungs the inhalation of 
tubercle-bacilli in considerable number may be followed by rapid 
tuberculous pneumonia without definite tubercles, and in other 
situations similar results maybe produced. In -the further prog- 
ress of a case of tuberculosis caseous change is important. This 
may present itself in the form of areas of considerable size having 
a dull, opaque, lusterless, grayish or whitish character, and not 
inaptly likened to the appearance of cheese. These centers of 
caseous necrosis may finally become liquefied, and cavity-forma- 
tions may result. These changes are particularly frequent in 
tuberculosis of the lungs, less frequent in bones, skin, glands, 
kidneys. In connection with tuberculosis of bones there may 
be formed small or large cavities filled with liquefied caseous 
or puriform material. These may involve the surrounding tis- 
sues as well as the bones themselves. The term cold abscess 
is applied to them. Small tubercular areas and sometimes even 
large foci are prone to be surrounded by reactive fibrous-tissue 
hyperplasia, and thus a complete encapsulation may result. Small 
foci may be uniformly transformed by organization of proliferating 
connective tissue and may be thus entirely healed. In other cases 
simple encapsulation occurs, the tuberculous mass within perhaps 
undergoing calcification. These changes will be more particularly 
referred to below. 

Tuberculous lesions of the mucous membranes frequently begin 



238 



TEXT-BOOK OF PATHOLOGY. 



with the formation of distinct tubercles occupying the deeper 
layers of the mucosa or the submucosa. These by confluence may 
form considerable areas of tuberculous disease, while at the same 
time reactive inflammation of the surrounding tissues adds to the 
mass. Sooner or later ulcerative changes upon the surface make 
their appearance and irregular, more or less necrotic, ulcers re- 
sult. The caseous appearance of these and the occurrence of 
distinct tubercles in the edges or base manifest the character of 
the process. 

Structure and Evolution of the Tubercle. — When the tubercle- 
bacillus is received into any tissue or organ its first effect, accord- 
ing to the investigations of Baumgarten, is to stimulate or irritate 
the fixed connective-tissue elements and cause a proliferation of 
round cells, which resemble in their abundance of protoplasm the 
epithelial cells, and are therefore known as epithelioid cells. These 




Fig. 92.— Miliary tubercles in the liver, showing abundant round cells in the peripheral 
parts, epithelioid and giant-cells within. 

have usually a single nucleus, of rather clear vesicular appear- 
ance, not deeply staining, and a relatively large amount of proto- 
plasm. They may be produced in greater or less abundance, as 
the first reactive change of the tissues to the irritation of tubercle- 
bacilli. Next there follows an infiltration with leukocytes from 
the surrounding blood-vessels, and the focus of irritation thus 
becomes surrounded with numerous small round cells mostly 
mononuclear, with darkly staining nucleus and a small protoplas- 
mic body (Fig. 92). Some of the cells are polynuclear. This 
leukocytic infiltration represents the reaction of the vascular sys- 
tem to the tuberculous irritation or infection. The number of small 
round cells varies greatly indifferent instances. Sometimes, as in 



BACTERIA AND DISEASES DUE TO BACTERIA. 239 



certain tubercles of lymphatic glands, they may be relatively few, 
while the epithelioid cells are present in abundance. In other 
cases the leukocytes are so quickly attracted and in such num- 
bers that the tubercle seems composed of these cells alone, no 
epithelioid cells appearing in view. These tubercles are known 
as the lymphoid. In the later stages the round cells may disap- 
pear by degeneration, exposing the previously hidden epithelioid 
cells to view. 

At the stage of the tubercle when it is composed mainly of 
epithelioid and lymphoid cells it appears to the naked eye as a 
grayish, somewhat translucent pearly body. It is avascular, no 
tendency toward formation of new blood-vessels being apparent. 
In the further evolution of the lesion degenerative changes take 
place. These are hyaline degeneration, coagulation-necrosis, fatty 
change, and eventually a transformation into cheesy material, 
the so-called caseous necrosis. These changes result from the 
specific action of the living tubercle-bacillus, though in part 
also from the avascular condition of the tissue. Avascularity 
alone, however, is not the cause of caseous necrosis. One 
of the first changes noted is a granular change in the cell- 
protoplasm which lessens the affinity of the cell-protoplasm 
and of the nucleus for ordinary stains. There may be 
seen among the cells of the tubercle here and there indi- 
viduals which show this beginning necrosis. These are usually 
grouped in the center of the tubercle, though at times also at dif- 
ferent points. The outlines of these cells become less distinct and 
they are progressively less deeply stained, until with advanced 
necrosis the cell is broken down into particles or debris (Fig. 93). 
In the early stages of necrosis the epithelioid cells tend to run 
together, forming large, irregular giant-eells with many nuclei 
arranged either around the periphery or frequently at either pole 
of the cell. Some observers believe that giant-cells result from 
rapid multiplication of nuclei within the epithelioid cells. This is 
very rare. Others have supposed that the running together of 
leukocytes or lymphoid elements of the tubercle causes the for- 
mation of giant-cells. This does not seem ever to occur. The 
giant-cell is not characteristic of tuberculosis, as it may be found 
in many of the specific inflammations and also in foci of chronic 
irritation due to foreign bodies, as well as in tumors. In no con- 
dition, however, are they so abundant or so conspicuous as in 
tuberculosis. In some cases they may not be seen in the tubercles 
at any stage. In other cases they are very numerous. The giant- 
cell falls an early victim to the advancing necrosis, and the pro- 
toplasm becomes granular and opaque, and eventually breaks down 
completely. This change usually occurs at the opposite side of 
the cell from that in which the nuclei are gathered ; or in cases in 
which the nuclei surround the cell the necrotic changes begin in 



240 



TEXT-BOOK OF PATHOLOGY. 



the center. Finally, a tubercle undergoes almost complete necrosis 
and is transformed into a cheesy mass, the surrounding connective 
tissue perhaps still showing proliferative changes which may 





Fig. 93.— Large tubercle of the lung, showing cheesy necrosis in the center ; the epithe- 
lioid and giant-cells around the cheesy center are more or less degenerated. 

eventually cause encapsulation of the tubercle. Calcification may 
ensue in the cheesy mass and thus lead to permanent destruction 
of the nodule. 

In the growth of tuberculosis the normal tissue-elements of the 
part affected are pushed aside, or may be softened and destroyed by 
the disease-processes. The connective-tissue fibers of the part, 
however, are longest retained, and remain as a reticulum or tuber- 
cle-stroma long after the other elements of the tissue have dis- 
appeared or been pushed aside. 

Tubercles tend to coalesce, forming larger tubercular masses, 
and sometimes distinct tuberculous tumors are so produced. In 
the lower animals, particularly in cattle, such tubercular tumors 
of the serous surfaces are not uncommon. They may simply 
stud the membranes, or they may hang as polypoid masses ; the 
term " pearl disease " is applied to these cases. Somewhat similar 
tubercular tumors are met with in human tuberculosis, especially 
in the brain. As a rule, however, increasing areas of tuberculous 
disease of organs are only partly composed of tubercles, the bulk 
of the diseased area presenting evidences of ordinary or peculiar 
inflammatory changes to which the presence of the tubercles has 
stimulated the tissues. 

The tubercle-bacilli in the earliest stages of the tubercle may 
be seen lying in the tissue and perhaps between the epithelioid 
cells first formed. With the evolution of the disease they are 



BACTERIA AND DISEASES DUE TO BACTERIA. 241 



more and more abundant, are largely within the cells, and the 
giant-cells in particular may contain large numbers (Fig. 94). As 




Fig. 94.— Giant-cell containing bacilli (from a photograph made by Dr. Wm. M. Gray). 

the necrotic changes increase the bacilli become less conspicuous, 
and eventually none may be visible. The existence of the bacilli 
or their spores, however, cannot be doubted, since injection of 
portions of such tubercles produces the disease in guinea-pigs. 

After the establishment of the local lesion of tuberculosis in 
any part of the body two opposing tendencies struggle for suprem- 
acy, the tendency of the tuberculous disease to spread and the 
tendency of the normal tissues to encapsulate or limit the spread 
of the invading disease. In most cases the former succeeds and 
the secondary tubercles first appear in adjacent parts, the transpor- 
tation of the bacilli from the primary to the secondary focus being 
accomplished either by the flow of the lymph or juices of the body, 
or by the phagocytic activity of leukocytes. The latter take from 
the edges of the tubercle some of the bacilli and transport them 
either by their own ameboid activities or in the lymph-stream to 
neighboring parts, where they themselves fall victims to the organ- 
isms they have appropriated, and thus deposit the germs of new 
foci of disease. The dissemination of tubercles to more distant 
parts may occur in various ways. In the case of tuberculosis of 
the mucous membranes bacilli may be cast off from the surface 
and spread to other parts of the mucous tracts with the contents 
of these, as in the case of tuberculosis of the gastro-intestinal 
tract. In the case of pulmonary lesions the ulcerative processes, 
or attacks of coughing, may loosen infected particles from lesions 
of the bronchi, and the deep inspiratory efforts following the 
cough, or the ordinary inspirations, may carry the bacilli into 
the finer bronchioles, where new foci arise. If the tubercular 
lesion involves the walls of the lymphatics, particularly the larger 
lymph-channels, like the cervical or thoracic ducts, bacilli may 

16 



242 



TEXT-BOOK OF PATHOLOGY. 



gain access to the lymph-stream and thus be transported to the 
venous circulation, and then through the heart to the lungs or 
perhaps to other organs. When the tuberculous lesion invades the 
wall of a vein the dissemination of the bacilli is even more rapid 
and widespread, as the organisms find their way to the heart by a 
more direct route. In rare instances an artery is invaded and the 
organisms are scattered through the terminal distribution of this. 
Upon surfaces the disease may spread by direct continuity or by 
the movements of the body. Thus lesions of the peritoneum may 
become almost universal in consequence of the peristaltic move- 
ments, though more frequently the extension occurs along the lym- 
phatic channels. 

The condition which results from general infection and forma- 
tion of tubercles in various situations is known as miliary tubercu- 
losis. In these cases the progress is usually rapid and a fatal 
termination is not long delayed. The tubercles therefore remain 
small, and at autopsy are still typically gray miliary tubercles. 
Sometimes, however, miliary tuberculosis may assume a more 
chronic form, perhaps in consequence of the gradual admission of 
bacilli to the circulation and the formation of small crops of 
tubercles during a considerable period of time. 

Miliary tuberculosis may be local or general. In the former 
case the bacilli are admitted to the vascular distribution of a re- 
stricted area only ; in the latter widespread dissemination through 
the blood occurs, and practically all parts of the body may be in- 
volved. Localized miliary tuberculosis is most frequent in the 
lungs. 

Seats of Tuberculosis. — Among the frequent situations 
in which tuberculosis makes its appearance are the lungs, the 
lymphatic glands, the bones and joints, the mucous membranes, 
particularly those of the larynx and intestines, the serous mem- 
branes, the prostate, testicle, ovaries, Fallopian tubes, kidneys, 
uterus, suprarenal capsules, brain, liver, spleen. In some of these 
situations the lesions are practically always secondary, as, for ex- 
ample, in the liver and spleen. In others they are most frequently 
primary, as in the lungs. The occurrence of primary tuberculosis 
in the internal organs may be difficult to explain. It is possible, 
however, for the bacilli to gain access to the lymphatic or blood- 
circulation without causing a lesion at the point of entrance. Their 
deposit in some internal organ then occasions the first or primary 
focus of disease. Thus primary tuberculosis of the mesenteric 
glands, of the lymphatic glands of the neck, or of the post- 
bronchial glands, may occur without primary disease of the intes- 
tines, of the mouth or skin, or of the lungs in the several instances. 
Similarly primary tuberculosis of the kidney or of the suprarenal 
capsule may occur without any evidence of the point of entrance 
of the micro-organisms. In some cases, of course, the primary 



BACTERIA AND DISEASES DUE TO BACTERIA. 



243 



lesion may be so small and in such a hidden situation that it 
escapes notice. 

After the discovery of the tubercle-bacillus a number of diseases 
not previously recognized as tuberculous became identified as 
forms of this disease. Among these is Lupus Vulgaris of the skin. 
The histologic examination shows numerous tuberculous granula- 
tions, sometimes arranged in striate fashion along the small blood- 
vessels of the skin and containing epithelioid and lymphoid cells 
and giant-cells. The presence of the bacilli and the proved infec- 
tiousness of the tissue, with the histology, render the nature of this 
disease certain. The warty formations frequently acquired by 
anatomists at points of injury have likewise been shown to be in 
many cases due to tuberculous infection. Scrofula, which was 
formerly regarded as a special condition predisposing strongly to 
tuberculosis, is now regarded as tuberculosis occurring in different 
forms and situations. The scrofulous glands of the neck consti- 
tute tuberculous adenitis, the infection in many cases gaining 
access through the mucous membranes of the mouth and pharynx 
or through the skin. Scrofulous rhinitis and sinuses have simi- 
larly been shown to be forms of tuberculous disease. Many cases 
of joint-disease regarded as scrofulous or otherwise are dependent 
upon the action of the tubercle-bacillus. 

The Smegma Bacillus. — A bacillus quite closely resembling the tubercle- 
bacillus was discovered in the smegma and later on the skin of various 
parts of the body. It not only resembles the tubercle-bacillus morpho- 
logically, but behaves in a similar manner toward stains. In particular this 
bacillus holds its stain when attempts are made to decolorize with acids. 
The bacillus is frequently found in urine, and thus may cause an erroneous 
diagnosis of tuberculosis of the kidney or bladder. It may usually, though 
not certainly, be distinguished by its easy discolorization with absolute 
alcohol. "Acid-proof" bacilli that have been found in milk and butter are 
probably identical or closely allied. The only certain means of differentia- 
tion is injection into guinea-pigs. 

Latent Tuberculosis. — A tuberculous lesion may become encap- 
sulated and limited in its extent before it has invaded tissues 
widely, and may so remain for years without giving rise to mani- 
fest clinical symptoms. Subsequently, however, the encapsulating 
membrane may be penetrated and widespread infection, local or 
general, may occur. Such latent tuberculosis is particularly fre- 
quent in the post-bronchial glands. These glands are often found 
enlarged at autopsies in which no tuberculous disease of other 
organs is found. Injections of emulsions of such glands in a nota- 
ble proportion of cases produce tuberculosis in guinea-pigs, and 
thus it has been determined that the glands in question are fre- 
quently the seat of latent tuberculous disease. The existence of 
such lesions explains the cases of sudden generalized miliary 
tuberculosis, in which no primary focus of the disease was recog- 
nized during; life. 



244 



TEX1-B00K OF PATHOLOGY. 



Pathologic Physiology.— The effect of tuberculosis upon 
the general health varies greatly. Undoubtedly the bacillus is 
capable of producing toxins that have an effect upon the general 
organism ; the nature of these, however, still remains undeter- 
mined. The tuberculin of Koch, a glycerin-extract from cultures 
of the tubercle-bacillus, produces fever with general symptoms 
such as are frequently associated with pyrexia and local reactive 
changes in existing tuberculous lesions. Among the latter redness 
or increased vascularization of the tubercles, and softening or ne- 
crosis of the cells surrounding the bacilli, are most important. The 
last-named change deters the growth and multiplication of the 
bacilli themselves, but at the same times makes their escape from 
the focus of disease more easy and thus exposes the individual to 
the liability of general infection. The active substance contained 
in tuberculin is probably an albuminous body. It does not act 
upon the tubercle-bacillus directly and is not an antitoxin. In 
addition to this the tubercle-bacillus in its dead state contains 
some body or bodies capable of influencing the organism, as was 
shown by the experiments of Prudden and Hodenpyl, who were 
able to produce nodular lesions and small local abscesses by in- 
jecting dead bacilli into the circulation of animals. These lesions, 
of course, are not strictly tuberculous, though they possess some 
elements of the natural tubercle. It is altogether probable, how- 
ever, that in addition to the tuberculin of Koch and the chemo- 
tactic substances contained in the body of the tubercle-bacilli, 
there are other poisonous substances produced by the growth and 
multiplication of the bacilli in the tissues, that lead to a general 
deterioration in the health of victims of this disease. 

Tuberculosis is primarily a local process, but influences the 
general organism by its direct effect upon the organic functions of 
the parts in which it is located by the development of these as yet 
unknown toxic substances, and later by the widespread infection 
of the organism. The mechanism of defence against tuberculosis 
is only partly known. In the case of local lesions of the lungs or 
other parts the reaction of the tissues probably resulting from the 
activity of chemotactic substances in the body of the bacilli them- 
selves, or of similar substances produced by the cellular necrosis, 
leads to the formation of an embankment of cellular or fibrous 
tissue that serves to hold the disease in check. Subsequently the 
disease may be wholly eradicated by degenerative changes termi- 
nating in calcification. That such favorable results are not 
uncommon is proved by the frequent occurrence at autopsies of 
small sclerotic or calcareous areas in the lungs. Tuberculosis is 
frequently cured in these early stages, but after it has reached the 
degree of intensity or the widespread character that makes it recog- 
nizable by our present methods of physical examination, the reactive 
processes are usually no longer able to cope with its progress. 



BACTERIA AND DISEASES DUE TO BACTERIA. 245 



FOWL=TUBERCULOSIS. 

Tuberculosis in various forms of fowl or birds (Avian Tuber- 
culosis, Tuberculosis Gallinarum) is a disease similar to, but not 
identical with, human tuberculosis. The spontaneous disease of 
birds occurs most frequently in the liver. There are nodules 
composed of round cells, but showing little tendency to coagula- 
tion-necrosis or to the formation of giant-cells. The bacillus, 
which is found in abundance, resembles the human tubercle- 
bacillus and may be stained by the same methods, but differs 
from this organism in the fact that it grows upon ordinary media 
and not upon potato, and is more resistant to heat, at least as far 
as its retention of virulence is concerned. The bacillus is more 
often club-shaped and branched than is the bacillus of human 
tuberculosis. When injected into the peritoneal cavity of birds, 
it causes in the liver and other abdominal organs lesions similar to 
those of the spontaneous disease. When inoculated in rabbits, 
abscesses result at the point of inoculation, and, later, lesions of 
the lungs develop. The lungs are never primarily involved in 
the spontaneous disease of birds. Many believe this disease a 
variety of tuberculosis modified by its occurrence in birds. 

PSEUDOTUBERCULOSIS. 

This name has been applied to conditions occasionally met 
with in which nodular lesions resembling tubercles, but containing 
micro-organisms of different kinds, have been found in the liver, 
kidneys, and other organs. One of the best studied of the organ- 
isms in question is a bacillus, non-motile, and easily stained by 
methods which do not color the tubercle-bacillus. The bacilli 
tend to arrange themselves in chain formations. 

Pueumonomycosis Aspergillina. — In man and in animals pulmonary infec- 
tion with forms of aspergillus, especially A. fumigatus, may occur in a 
pseudotuberculous form. The lesions are exudative and proliferative, and 
central caseation may be conspicuous. The fungi which belong to the 
group of hyphomycetes are readily distinguished by the abundant mycelial 
threads and the conidia. Infection of other organs may occur sponta- 
neously or experimentally. 

Pure cultures inoculated in other animals give rise to the same 
lesions. Pseudotuberculosis is probably not a specific form of 
disease ; a variety of conditions may present this appearance. 

LEPROSY. 

Definition. — Leprosy, Lepra, or Elephantiasis Grsecorum, is 
an infectious and mildly contagious disease caused by a specific 
bacillus, the Bacillus leprae, discovered by Hansen. 

Ktiology. — The essential cause of leprosy is a bacillus which 



246 



TEXT-BOOK OF PATHOLOGY. 



closely resembles the tubercle-bacillus, though it is less frequently 
curved and is somewhat more easily stained. Further, it differs 
in its grouping in the tissues and in its failure to grow satisfac- 
torily on artificial media. The organism is usually found in large 
numbers in the leprous lesion aud in the nasal mucus, whether 
there be definite leprous ulcerations in the nose or not. It is 
readily stained by any of the methods applicable for the tubercle- 
bacilli or by Gram's method. It frequently shows light areas 
like those of the tubercle-bacillus, and these have been regarded 
as spores ; more probably they are produced by fragmentations, 
as in the case of the tubercle-bacillus. Attempts at culture have 
thus far been unsuccessful, though Neisser claims to have ob- 
tained cultures on blood-serum containing gelatin and on coagu- 
lated egg-albumin. Others have claimed definite results with 
similar media, but cultivation at the present time is not ordinarily 
possible. 

The specific nature of the bacillus has not been demonstrated, 
as it is almost, if not entirely, impossible to produce the disease 
in animals. Some successful experiments have been made by 
inoculating portions of leprous tissue in the anterior chamber of 
the eye or other parts of animals ; but definite generalized leprosy 
has not been thus far produced. In one case the disease has been 
given to a condemned criminal by direct inoculation. 

Besides the specific bacillus other conditions are important in 
the etiology. Thus the disease flourishes in certain localities 
extensively and little in other places. It is uncommon in the 
United States, but some of the Gulf States, particularly Louisiana, 
have considerable colonies, and in the Northwest and on the Pacific 
Coast it is met with among the Norwegian and Chinese immi- 
grants. In Mexico, South America, Norway and Sweden, India, 
and other Asian countries it is common, and the Sandwich Islands 
are particularly affected. During the Middle Ages it flourished in 
Europe as a universal scourge, unsanitary conditions probably 
acting as the predisposing cause. Certain articles of diet are 
believed to occasion it, particularly fish ; this view, however, lacks 
proof. 

The disease must be regarded as contagious, though less so 
than tuberculosis. Intimate association for a long time seems to 
be necessary for its transference. It is probably transmitted from 
parent to offspring in rare instances. 

Pathologic Anatomy. — Leprosy presents itself in two 
forms, the tubercular and the anesthetic form. In the former there 
are developed in the skin of the face, the extensor surfaces of the 
elbows and knees, about the hands, or less frequently elsewhere, 
small or large nodular elevations. These at first are reddish in 
color, with apparent inflammatory reaction. Later they lose their 
redness and remain as indolent lesions that grow very slowly or 



BACTERIA AND DISEASES DUE TO BACTERIA. 



247 



remain stationary. They may break clown, forming ulcerations 
which do not readily heal, or they may be gradually converted 
into fibrous cicatricial tissue, causing unsightly deformities of the 
skin. The appearance of the patient's face is highly characteristic, 
and is known as leontiasis leprosa (Fig. 95). The mucous mem- 




Fig. 95.— Nodular leprosy (Goldschmidt). 



branes and some of the internal organs may be involved. The 
anesthetic form is usually marked by less conspicuous lesions, but 
subjective symptoms, such as hyperesthesia and neuralgic pains, 
and later ulcerations partly tr >phic in nature, may make it a more 
serious variety. In the skin there are found whitish or brownish 
spots, slightly if at all elevated or altered in consistency. Later, 
ulcerations may appear. Very commonly the anesthetic and 
tubercular varieties are coexistent. 

The nodules occurring in the liver, spleen, and testes in this 
disease are admitted to be similar to the nodules of the skin ; 
those found in the lungs, kidneys, and intestines, as well as those 
of the serous surfaces, are believed by many to be tuberculous and 



248 



TEXT-BOOK OF PATHOLOGY. 



the result of secondary infection. These two diseases are certainly 
frequently associated ; probably 40 per cent, of the cases of lepra 
become tuberculous. 

Other forms of secondary infection occur, thus injuries of 
superficial lesions may allow pyogenic infection, and extensive 
ulcerations and gangrenous necrosis may ensue. The terms lepra 
mutilans and lepra gangrenosa are applied to such ; and various 
micrococci and saprophytic organisms have been discovered in 
such cases. 

Structure of the Leprous Lesions. — The nodule or leproma is a 
somewhat indurated growth resembling the tubercle, but differing 
from it in its greater vascularity and in the absence of the ten- 
dency to cheesy necrosis. Microscopically it is composed very 
largely of proliferated connective-tissue cells of different forms, 
and leukocytes. New blood-vessels are discovered in more or less 
abundance, and a tendency to complete organization with the 
formation of fibrous tissue may be seen in the character of the 
cells and the presence of fibrous intercellular material. The 
bacilli occur within the cells and possibly also between them. 
They are always found in groups and usually in large numbers. 
They multiply within the cells, the protoplasm of the latter at the 
same time undergoing a process of swelling and degeneration. 
This at first spares the nucleus, but finally the nucleus itself is 
broken down and the cell is thus converted into a sac -containing 
degenerated protoplasm and abundant bacilli (Fig. 96). The 

term lepra-cell has been given to these. 
Giant-cells may be formed, though they 
are not frequent and are rarely typical. 
Secondary infections or injuries may lead 
to suppurative or other forms of soften- 
ing, and the final termination either with 
jt* or without previous softening may be 

cicatrization. The lesions of the internal 
organs met with in some leprous cases, 
notably those of the lungs, intestine, kid- 
ney, and serous surfaces, are avascular, 
ie P S G cen \Ka?rand a schm*i) a show more tendency to necrosis, and con- 
tain more giant-cells ; in some cases inoc- 
ulation has showed that the lesions contained tubercle-bacilli. 
Whether they are strictly tubercles, or whether they are lepro- 
mata with secondary infection with tubercle-bacilli, cannot be 
decided. They are certainly not pure leprosy, and more probably 
are purely tuberculous. 

The anesthetic areas and pigmented or light-colored spots of 
the anesthetic form present somewhat the same histologic features 
as the leprous nodule, though in a diffuse form. Formerly these 
lesions were considered entirely the result of trophic changes. 




BACTERIA AND DISEASES DUE TO BACTERIA. 249 



In these cases the more conspicuous lesion is that of the nerves. 
These may show nodular thickening of the perineurium with inflam- 
matory and degenerative changes of the nerve itself. The bacilli 
are present in these lesions. Changes in the spinal cord have 
occasionally been discovered. 

Pathologic Physiology. — Infection with the lepra-bacillus 
leads to local rather than general disturbances. The toxins of the 
disease, if such there be, are not of great virulence, and constitu- 
tional symptoms are therefore wanting as a rule. In the later 
stages fever and other systemic disorders may be occasioned by 
secondary infections. A supposed antitoxic substance has been 
prepared and has been largely used. It is impossible to claim or 
disclaim the antitoxic nature of this, as no toxins have as yet been 
isolated or obtained in any form, and the supposed antitoxic sub- 
stances cannot therefore be tested. 

In the anesthetic form it was formerly customary to regard the 
pigment or light-colored spots as a result of trophic disturbance, 
and more destructive lesions, such as ulceration and gangrene, 
received a similar explanation. Recent investigations, however, 
seem to show that in these cases there is usually from the first a 
leprous change in the tissues, and that secondary infections fre- 
quently play a part, though trophic disturbances must still be 
admitted to a certain extent. 



GLANDERS. 

Definition. — Glanders is an infectious and contagious disease 
of horses and asses, sometimes communicated to other animals and 
to man, and caused by a specific bacillus. 

Etiology. — The Bacillus mallei was discovered by Loffler and 
Schiitz. It is an organism resembling the tubercle-bacillus, 
though somewhat shorter and thicker. It occurs in the lesions of 
the disease singly or in clumps, and has been found in the blood. 
The bacillus is non-motile and does not possess flagella. Stained 
specimens show parts that do not receive the stain. These have 
been regarded as spores, but are more generally thought to be areas 
of degeneration. Ordinary solutions of anilin dyes, and especially 
alkaline solutions, stain the organism very well. The demonstra- 
tion of the bacillus in the tissues requires prolonged staining and 
rapid decolorization. 

Cultivation. — Cultures are best obtained from softened nodules 
of guinea-pigs inoculated with infected pus, or from the testicles 
after injection of infective matter into the peritoneal cavity. The 
organism grows quite readily upon ordinary media, but the most 
characteristic culture is seen upon boiled potato. The colony 
first appears as a honey-like layer, which becomes brownish in 



250 



TEXT-BOOK OF PATHOLOGY. 



color. The potato itself becomes greenish-brown beneath and 
around the colonv. The cultivation is most successful between 
30° and 40° C. (86° and 104° F.). 

Drying and elevated temperatures rapidly destroy the organ- 
ism, and antiseptics kill it quite readily. The bacillus is a pure 
parasite, multiplying only in the body of infected animals or 
man. 

Pathogenicity. — The specific character of the bacillus is unques- 
tionable. Inoculation of guinea-pigs, rabbits, field-mice, or other 
animals with infected pus or with pure cultures leads to nodular 
lesions at the point of introduction, with subsequent softening and 
ulceration. After death nodules are found in the liver, spleen, 
kidneys, or other organs, and these contain the bacilli. In horses 
and asses characteristic lesions of the mucous membranes have 
been produced experimentally ; while in man accidental infection 
of hostlers or others coming in contact with diseased animals, and 
of bacteriologists working with cultures, has been repeatedly 
observed. In one case in my own knowledge a man was infected 
in a stable in which a glandered horse was kept, and the bacteri- 
ologist who isolated the organisms from the patient accidentally 
infected himself with the cultures. 

Pathologic Anatomy. — In horses glanders presents charac- 
teristic lesions of the mucosa of the nose. At first there are found 
slightly elevated nodules, which have a marked tendency to soften, 
forming irregular ulcerations that become confluent. The floor 
and edges of the ulcers are yellowish and necrotic in appearance, 
and discharge more or less purulent matter. The lymphatic glands 
of the neck and elsewhere enlarge and may suppurate. In the 
skin the lesions are much the same, but more sluggish. JNodules 
are not rarely met with in the lungs. These are grayish or pink- 
ish in color, and tend to rapid necrosis. More rarely nodules or 
ulcers are found in the mucosa of the gastro-intestinal tract. 

In man similar nodules and ulcerations may be found in the 
nose, larynx, or trachea ; and external lesions resembling small or 
large carbuncles are found. 

Histologically the lesions of glanders consist of aggregations 
of round cells of lymphoid or polymorphonuclear type. There is 
a marked tendency to suppurative or necrotic softening, and some- 
times hemorrhagic infiltration may be pronounced. 

Pathologic Physiology. — A toxic substance called mallein 
(a bacterial protein) has been obtained from cultures of the bacilli. 
Injected into infected animals this acts somewhat as does tubercu- 
lin in tuberculosis. A special toxin is probably active in the pro- 
duction of the general symptoms of the disease. By repeated 
dosage with mallein it is claimed that immunity may be con- 
ferred. 



BACTERIA AND DISEASES DUE TO BACTERIA. 251 



MALIGNANT EDEMA. 

Definition. — Malignant edema is a form of intense infective 
inflammation and necrosis observed in certain animals and in man, 
and is due to a specific micro-organism. The condition has fre- 
quently been described by clinicians as gaseous gangrene, traumatic 
gangrene, gangrene foudroyante, etc. Infectious emphysema (g. v.) 
has doubtless often been mistaken for this disease. 

etiology. — The micro-organism of malignant edema was de- 
scribed by Pasteur and named the Vibrion septique. Koch showed 
that it does not flourish in the blood, and that the name given by 
Pasteur is therefore not appropriate. He therefore named it Ba- 
cillus osdematis maligni. This organism is widely distributed. It 
is very commonly present in the soil, particularly in garden-earth, 
and is often found in dust and in the intestinal contents of animals. 
Introduced into the subcutaneous tissue of animals it multiplies 
greatly and sets up a violent local process. The 
bacilli are readily obtained from the diseased 
area, and may be stained with the ordinary 
anilin dyes, but not by Gram's method. The 
bacillus resembles the anthrax-bacillus very 
closely, but is somewhat more slender. It is 
prone to occur in long chains, the organisms 
being apparently in contact end to end. Move- 
ment of the organisms is frequently observed, and 
lateral flagella are found by appropriate stains. 
In the spore-formation the center of the organ- 
ism swells and the spore is developed within. 

Cultivation. — The cultivation of this organ- 
ism is generally easy. White mice or other sus- 
ceptible animals are first infected by introducing 
powdered garden-earth into a subcutaneous sac. 
Direct infection of the open wound will not suc- 
ceed, as the organism is strictly anaerobic. 

From the pus in the subcutaneous tissues 
growths may be obtained upon the surface of 
gelatin in an atmosphere of hydrogen, or in 
puncture-cultures in gelatin from which oxygen 
has been excluded. On the surface of the gela- 
tin are formed small grayish-white bodies, which 
increase in size with advancing age. Portions 
removed from these and stained show masses 
of bacilli in the form of long filaments. In the 
gelatin-tube there are formed whitish spherical 
colonies of a somewhat cloudy appearance. These consist of a turbid 
liquid, the gelatin undergoing liquefaction. There is also some 
gas-production, the gas formed having a peculiar and unpleasant 
odor. This is marked when the medium contains glucose (Fig. 97). 



f 



Fig. 97.— Bacillus 
of malignant edema 
growing in glucose- 
gelatin" (Frankel and 
Pfeiffer). 



252 



TEXT-BOOK OF PATHOLOGY. 



Distribution. — The bacillus ' of malignant edema occurs only in 
the subcutaneous tissues near the point of inoculation, in the mus- 
cles, and in the peritoneal cavity at the time of death. It does 
not invade the blood, as the amount of oxygen there present pre- 
vents its growth, and it flourishes in the subcutaneous tissue 
because this is least accessible to oxygen. In bodies dead some 
time the organism may spread to the blood and the organs of the 
body. The distribution of the organisms outside the body has 
been referred to. 

Pathogenicity. — The bacillus of malignant edema is undoubtedly 
the cause of the disease in question, as has been proved by inocu- 
lations upon mice, guinea-pigs, and other animals. Cats and dogs 
are less susceptible than other animals ; cattle seem to be almost 
wholly immune. 

Pathologic Anatomy. — The lesions of malignant edema 
consist of various forms of rapid suppuration and necrotic in- 
flammation of the subcutaneous tissues. There may rapidly form 
emphysematous and gangrenous alterations of the subcutaneous 
tissues, with sometimes pus-formation, at other times extensive 
hemorrhagic infiltration. 

Pathologic Physiology. — Toxins are doubtless formed, but 
these have not as yet received special attention. Artificial im- 
munity has been secured by injections of sterilized cultures of the 
bacillus in bouillon, and by other methods. A few cases of malig- 
nant edema have been reported in man, some following injection 
of musk in the course of typhoid fever, some occurring in the 
puerperium, and some apparently without external injury. Infec- 
tion in the latter probably occurred from the mucous surfaces. In 
all cases the general vitality of the patient was reduced by some 
previous disease. 

ANTHRAX. 

Definition. — Anthrax is a specific infection due to a charac- 
teristic bacillus. It occurs most frequently in cows and sheep ; it 
may affect other animals and man. Dogs, cats, birds, and cold- 
blooded animals are quite immune. In animals it is called splenic 
fever ; in man, malignant pustule and wool-sorters' disease. 

Etiology. — The Bacillus anthracis is a non-motile rod-shaped 
organism that has a decided tendency to form long chains. The 
individual bacillus is from 5 to 20 fi in length and from 1 to 1.25 ti 
in thickness. The chains appear as threads, with often a little 
thickening at the ends of the individual bacilli showing the points 
of contact. The ends are squared or often slightly concave. In 
artificial cultures in the presence of oxygen spores are formed 
within the bacilli. These are elliptical or oval in shape, and do 
not alter the configuration of the bacillus (Fig. 98). 



BACTERIA AND DISEASES DUE TO BACTERIA. 253 



The organism is easily stained with the simple anilin dyes, and 
may be demonstrated in the blood or the tissues by Gram's or 
Weigert's stains. There are no flagella. 

Cultivation. — The anthrax-bacillus may be obtained in pure 
culture from the diseased organs upon various media. The cul- 
ture in gelatin is most characteristic. Upon plates there are 
formed whitish colonies, which under low powers of the micro- 
scope show a tufted, irregular character at the edges and upon the 
surface, suggesting bunches of twisted wool-fibers. The gelatin is 
slightly liquefied. The tufts may be removed by pressing a cover- 
glass against the surface of the colony, and when stained are found 
to consist of curved parallel chains of bacilli. In puncture- 
cultures filaments project at right angles to the puncture toward 




Fig. 98.— Bacillus anthracis, stained to show the spores (Frankel and Pfeiffer). 

the sides of the test-tube, and the growth at the surface, where 
oxygen is abundant, is luxuriant, while that in the depth is com- 
paratively sparse. 

Pathogenicity. — The infectiveness of the bacillus is undoubted. 
A small portion introduced into a susceptible animal gives rise to 4 
marked symptoms in twelve or twenty-four hours, and death soon 
follows. The bacilli may be demonstrated in the blood and in 
various organs in great abundance. When the bacillus is killed 
and the spores are introduced into the body similar results follow. 

Distribution. — The anthrax-bacillus occurs in all of the local 
lesions, and from these extends into the blood and into the organs, 
particularly the spleen, liver, kidney, and lungs, where it is 
found in the capillaries in immense numbers. The structure of 
these organs is, as a rule, little affected, probably because death 
occurs before changes may take place. The organisms are dis- 



254 



TEXT-BOOK OF PATHOLOGY. 



charged from the body in the stools, urine, and other discharges, 
and thus conveyed to other animals. At one time it was sup- 
posed that they are scattered about by earth-worms obtaining 
them from cadavers. This is scarcely probable. Multiplication 
of the organisms outside the body does not occur to any extent, 
but the organisms, and particularly the spores, may live a long 
time, and may be conveyed to great distances in infected mate- 
rials, particularly wool, hides, bristles, and the like. 

Mode of Infection. — In animals infection most frequently occurs 
through the gastro-intestinal tract, the bacilli being swallowed 
with fodder that has been contaminated. The organisms may, 
however, gain entrance through the lungs or through external 
abrasions. The latter form of infection is most common in 
man ; though gastro-intestinal and pulmonary infection sometimes 
occurs. 

Pathologic Anatomy. — The lesions produced by anthrax 
are more or less local, but occasion general septicemia. In man, 
after infection of the skin through abrasions in persons handling 
the hides or w r ool, or other materials from diseased animals, a 
swelling of greater or less size develops. This is intensely in- 
flammatory, often covered and surrounded by slight bullous vesi- 
cles, and attended with considerable edema. Erosion of the sur- 
face may take place and sanious liquid may be discharged, with 
the formation of crusts. Histologically the process consists of 
rapid infiltration of the corium and papillary bodies with leuko- 
cytes. The bacilli are found in abundance between the cells, and 
hemorrhagic infiltration and sero-sanguinolent edema are observed. 
Necrosis subsequently occurs, though not to a considerable extent. 
When infection takes place through the gastro-intestinal tract, as 
is sometimes observed in man and very commonly in animals, 
lesions somewhat like the above are formed in the mucosa 
and submucosa of the small intestine, less frequently of other 
parts. At first these lesions appear as hemorrhagic extravasa- 
tions, then swelling follows, and finally the surface ulcerates, leav- 
ing irregular excavations with blood-stained bases and edges. 
Profuse diarrhea with bloody discharges may occur. Infection 
through the lungs occurs in men engaged in handling infected 
wool (wool-sorters' disease), and in persons working in paper-fac- 
tories, where infected rags carry the germs. In these instances 
the bacilli lodge in the alveoli of the lungs, causing rapid cellular 
exudation with considerable edema and hemorrhagic infiltration. 
The process is lobular in character, but large areas of the lungs 
may be simultaneously involved. Serosanguinolent pleurisy, swell- 
ing of the lymphatic glands of the mediastinum, and hemorrhagic 
extravasations of the mediastinum are not unusual. 

Pathologic Physiology. — The presence of the anthrax- 
bacillus leads to the formation of toxic materials in the blood, and 



BACTERIA AND DISEASES DUE TO BACTERIA. 255 



a poisonous albumose has been obtained from cultures. The 
general symptoms, however, are probably in large measure the 
result of dissemination of the bacilli themselves and their local 
effects. 

It has been found possible by cultivation at high temperatures 
and by introducing the organisms into insusceptible animals, and 
also by adding chemical agents to cultures, to alter the pathogenic- 
ity of the bacillus to such an extent as to make it harmless, even 
to white mice. By introduction of such cultures and subsequent 
successive inoculation with cultures of increasing virulence pro- 
tection has been afforded. Antitoxic substances have been obtained 
from the blood of protected animals, but the method of successive 
vaccinations rather than the use of antitoxic serum is at present 
relied upon to combat the disease. 

INFECTIOUS EMPHYSEMA. 

Definition. — This term is provisionally applied to a form 
of infection that has been described under various names, such as 
gaseous gangrene, gas-phlegmon, emphysematous necrosis, and the 
like. Undoubtedly it has been mistaken for malignant edema in 
certain cases. The disease is caused by the Bacillus aerogenes 
capsulatus of Welch and Nuttall. 

Etiology. — The bacillus in question is a non-motile organism 
of variable size, 3 to 6 fx in length and about the thickness of an 
anthrax bacillus, with adjacent ends slightly rounded or square 
cut, and occurring singly, in pairs, clumps, or sometimes in short 
chains. Very rarely it occurs in long threads. It is easily stained 
with the ordinary anilin dyes or Gram's stain. A capsule is some- 
times demonstrable in specimens obtained from the body or 
from agar-cultures. The bacillus does not form spores. It is 
probably identical with the Bacillus phlegmones emphysematosa? 
of Frankel. 

Cultivation. — The organism is anaerobic, no growth occurring 
on the surface of solid media in the presence of oxygen. In 
media containing fermentable material gas-formation is regularly 
observed. The colonies in agar are grayish-white or slightly 
brownish ; those in the depth appearing as small spheres or ovals 
slightly flattened, Avith knob-like or feathery projections. The 
cultures in gelatin show slight and slowly developing liquefac- 
tion. 

Pathogenicity. — By experiments on animals exactly the same 
lesions are produced as those found in man. 

Pathologic Anatomy. — The lesions of this infection are 
widespread. At the point of inoculation there may be found 
edematous infiltration, with blood-stained fluid, and emphysema 
due to gas-formation. Rapid necrosis or gangrenous soften- 



256 



TEXT-BOOK OF PATHOLOGY. 



ing of the tissue may occur. The entire surface of the body 
sometimes becomes emphysematous, and at the autopsy the organs, 
especially the myocardium, kidneys, liver, and spleen, present a 
characteristic appearance. They are lighter in color, and on in- 
spection are found to be filled with minute vacuoles or gas-bub- 
bles. The blood of the heart and vessels presents a foamy condi- 
tion, due to the gas-formation. Practically any of the tissues of 
the body may be affected. Microscopically, the occurrence of gas- 
vesicles with numerous bacilli in their walls is the most striking 
feature. 

Regarding the mode of infection, it seems likely that in all 
cases the organisms enter through some injury or abrasion con- 
nected with the external world. Some cases have followed trau- 
matic injuries, others occur in connection with disease marked by 
ulcerations of the surface of mucous membranes, and at least one 
instance has been carefully studied in which the disease occurred 
during the puerperium, probably due to uterine infection. It is 
not improbable that many of the cases of supposed air-embolism 
from douching of the uterus after labor are in reality cases of 
this form of infection. 

TETANUS. 

Definition. — Tetanus is an acute infectious disease due to a 
specific bacillus. The bacillus of tetanus was discovered by Nico- 
laier and isolated by Kitasato. 

Etiology. — The bacilli occur in the form of cylindrical rods, 




Fig. 99— Bacillus tetani ; X 1000 (Frankel and Pfeiffer). 

which are frequently swollen at one end, due to the presence of a 
rounded spore (Fig. 99). They are slightly motile in the absence 



BACTERIA AND DISEASES DUE TO BACTERIA. 



257 



of air, and they may have flagella. They usually occur singly, 
though occasionally a few may be seen end to end. They 
occur in the local lesions from which traumatic tetanus takes its 
origin, and may sometimes be readily demonstrated by spreading 
some of the pus or exudate upon a cover-glass and staining with 
the ordinary anilin stains. They also stain by Gram's method. 
The bacillus does not diffuse itself through the body, but in a few 
cases it has been found in the central nervous system. The organ- 
ism is readily destroyed by heat, but its spores are quite resistant. 

Cultivation of the tetanus-bacillus is difficult. It is obtained 
from garden-earth or the pus of infected wounds by submitting 
the material to sufficient heat to destroy other organisms, even the 
bacillus of tetanus itself, leaving the spores uninjured. With this 
material animals are inoculated, and from the products of the local 
lesions or directly from the original material cultures are made in 
gelatin. 

The organism is strictly anaerobic. The typical culture is 
obtained in the depth of gelatin. Deep beneath the surface there 
are formed along the line of puncture pointed processes stand- 
ing out at right angles from the puncture. After a week lique- 
faction of the gelatin occurs, and an accumulation containing 
grayish-white turbid liquid is formed. When the growth is formed 
on the surface of gelatin in an atmosphere of hydrogen a similar 
radiating structure is found in the colonies, the centers of which 
are rather dense. Liquefaction of the gelatin subsequently takes 
place. Considerable gas with a pungent odor is produced in the 
growth of this bacillus. 

Distribution. — The tetanus-bacillus is found very frequently in 
garden-earth, in the intestinal discharges of animals, and upon 
various articles about stables. . Infection occurs in human beings 
or animals through punctures made by nails, splinters, and the like. 

Pathogenicity. — The bacillus placed upon an open wound may 
not give rise to the disease, from the fact that the presence 
of oxygen prevents its growth. Subcutaneous inoculation, how- 
ever, causes rapid destruction of animals with typical symptoms. 
The period of incubation may be only a few hours, or one or two 
days, or it may be several weeks. The association of certain 
other organisms, such as the pus-producing organisms, seems to 
favor the development of the disease by preventing phagocytic 
action of leukocytes, or by consuming oxygen and thus allowing 
the tetanus-bacillus to flourish. 

Pathologic Anatomy. — No characteristic lesions are found 
in this disease. Locally a wound or injury through which inocu- 
lation has taken place may be discovered ; but this is only excep- 
tionally extensive. Sometimes no local injury can be discovered, 
and it is supposed that infection at times occurs through the gastro- 
intestinal tract, or through other mucous membranes. Intense 

17 



258 



TEXT-BOOK OF PATHOLOGY. 



congestion of parts of the nervous system may he found at the 
autopsy, hut this is not characteristic. 

Pathologic Physiology. — Tetanus is essentially a toxemic 
disease. The bacillus produces, at the point of its growth, poisons 
of almost inconceivable power. Two distinct substances have 
been isolated, tetanin and tetanotoxin. These occur in the blood, 
urine, and probably other fluids of the body. The bacilli are 
not found in these fluids. When the toxin of tetanus is intro- 
duced into animals in gradually increasing quantity immunity is 
developed and the serum is found to have antitoxic power. The 
antitoxin may be precipitated from the blood by alcohol, and kept 
in a dry state. In practical medicine the antitoxin of tetanus has 
not proved as useful as experiments seemed to promise. This may 
be due to the fact that the intoxication is generally so extensive 
by the time the disease is recognized that treatment comes too late. 

ACTINOMYCOSIS. 

Definition. — Actinomycosis is a chronic infectious process 
characterized by inflammatory reaction of the tissues with a ten- 
dency to the formation of suppurative foci, and due to the specific 
action of a micro-organism, the Streptothrix actinomyces. 

Etiology. — Actinomycosis is a disease of cattle, horses, swine, 
and occasionally of man. 

The specific cause of the disease is an organism which occurs 
in the tissues in the form of clusters having a radiate structure, 
and it has therefore been termed the " ray fungus." These 
clusters may be so small as to be invisible to the naked eye, or 
they may reach considerable dimensions by their growth and 
aggregation. The central part of the cluster frequently has a 
granular appearance, suggesting a mass of micrococci. Reaching 
out from this may be seen more or less regularly diverging striae 
or rays, and the periphery is composed of what appear to be 
bulbous extremities of the rays (Fig. 100). 

The exact biologic position of the organism has not yet been 
determined. By some it is regarded as one of the hyphomycetes ; 
others place it among the bacilli. It is best classified as one of 
the sir eptothr ices, a group forming a link between moulds and 
bacteria. These are filamentous organisms which form mycelia 
and divide by budding. The mycelia tend to fragment, and form 
bodies resembling cocci, bacilli, etc. 

Cultivation of the Organism. — Two forms of cultures have been 
obtained from the lesions of actinomycosis of man and animals. 
These have certain resemblances, but differ so widely that they 
are regarded by many as distinct organisms. General considera- 
tions, however, would seem to indicate that they are sub-varieties. 

1. The important form is rigidly anaerobic. Cultures have 
been obtained upon agar and in hens' eggs. On the surface of 



BACTERIA AND DISEASES DUE TO BACTERIA. 259 



agar at 37° C. small colonies, resembling dewdrops, develop. 
These grow slowly, but remain distinct, and gradually become 
opaque. In addition to these, more distinct white nodules may 
form. These have an irregular periphery with outgrowths, and 
also present root-like projections into the depth of the agar. In 
the raw or quickly boiled egg, small whitish dots are formed 
without gas-formation or putrefaction. Microscopically, the organ- 
ism presents itself in the form of slender or thick rods, often 
curved, and sometimes a little swollen at the ends, but never club- 
shaped, like the rays of the fungus in the pathologic lesions. In 
addition, various coccus-like structures are found, and some wavy 
filaments. The small rods resemble closely the diphtheria bacillus. 

2. The second and less important form of culture grows best 
in the presence of air. Upon gelatin or agar plates radiating 
colonies which become opaque nodules are formed. On blood- 




Fig. 100.— Actinomyces cluster (Karg and Schinorl). 

serum and potato the growth is apt to be reddish in color, but is 
covered with a whitish down composed of air-hyphse. Old 
cultures present a dry and wrinkled appearance. Microscopically, 
the organism from such cultures appears in the form of long fila- 
ments with branches. Enlargements of the ends of the filaments, 
somewhat club-shaped in character, may be seen. 

Pathogenicity. — The anaerobic culture alone is pathogenic. 
Injection of pure cultures into the peritoneal cavity of guinea- 
pigs, rabbits, and other animals is followed by the development 
of typical lesions which are infectious when implanted in a second 
series of animals, and from which pure cultures may again be 
obtained. The aerobic culture is non-pathogenic. 

The manner of infection with the actinomycoses is not com- 
pletely determined. It is quite likely, however, that the parasite 
is carried to the tissues by various vegetable substances, particu- 
larly the spears of the oat-seed and other grains. Sometimes these 



260 



TEXT-BOOK OF PATHOLOGY. 



have been found embedded in the lesions ; in other cases splinters 
of wood have been discovered. It seems possible that the specific 
agent is conveyed into the tissues by these foreign bodies. 
Carious teeth doubtless play a part in the etiology. 

Pathologic Anatomy. — The pathologic changes induced by 
the actinomyces consist of round-celled infiltration and prolifera- 
tive changes in the connective tissue surrounding the parasite, and 
sometimes secondary softening, necrosis, or suppuration. In cattle 
the disease affects the lower jaw, less frequently the upper jaw or 
other bones ; the tissues of the neck, the tongue, and other parts. 
In man it is met with in the gums and floor of the mouth, in the 
lungs, intestines, and other internal organs. The naked-eye 
appearance of the lesions may first be simply that of a hard red 
papular formation, with more or less induration surrounding it ; 
later this tends to increase in size and may break down, forming 
necrotic or suppurative excavations. The process of repair or 
cicatrization may proceed in some parts to the extent of almost 
complete repair, while the suppurative or necrotic change advances 
in other directions, and thus cavities and irregular communicating 
sinuses are established. The part in which the disease exists may 
be considerably disfigured and much enlarged. The pus or 
necrotic material within the lesions has a peculiar granular charac- 
ter, the granules or actinomycosis-bodies frequently containing a 
group of the organisms. Occasionally calcification of the diseased 
area may take place. When the jaw-bone is affected the disease, 
as a rule, begins about carious teeth, fistulse communicating with 
the roots of teeth. 

In the case of disease of the lungs some have observed a pre- 
liminary catarrhal inflammation of the bronchi. More frequently, 
however, there are from the first nodular areas of bronchopneu- 
monia, which tend to undergo changes similar to those already 
described. The surrounding lung-tissue frequently becomes indu- 
rated from interstitial pneumonitis. Extension may occur to the 
pleura, pericardium, and mediastinal tissues. 

In the case of actinomycosis of the intestinal tract there are 
first elevations of the mucous membrane, the disease involving the 
mucosa and the submucosa. Subsequent softening of these leads 
to the formation of ulcerations. Extension to the peritoneum and 
to the other organs of the abdomen may take place. 

In any case of actinomycosis a penetration of the blood-vessels 
or lymph-channels may lead to metastases. Thus in actinomyco- 
sis of the abdominal cavity the liver is frequently involved ; and 
other parts of the body may be similarly affected. Actinomycotic 
lesions of the brain (abscesses) are sometimes seen in such in- 
stances. In other cases of cerebral involvement there may be no 
evidence of the original focus or point of entrance of the germ. 

Microscopically the characteristic feature of this disease is the 
parasite itself surrounded by lymphoid cells in considerable num- 



BACTERIA AXD DISEASES DUE TO BACTERIA. 261 



bers, with some epithelioid cells and occasionally giant-cells. 
When the process tends to a favorable termination by cicatrization 
fibrous-tissue formation proceeds in the usual manner. 

Pathologic Physiology. — The actinomyces is mainly active 
as a local parasite, the general disturbances of health being com- 
paratively slight. There is a marked tendency to limitation or 
retardation of the disease, and sometimes this is effected com- 
pletely. 

MYCETOMA. 

Mycetoma, or Madura-foot, is an infectious disease occurring in 
India and elsewhere, and caused by an organism of an uncertain 
biologic class. The disease is not infrequent in Madura, Delhi, 
and other parts of India, and has been observed in Africa, South- 
ern Europe, and America. 

Etiology and Pathologic Anatomy. — As its name indi- 
cates, the disease affects the foot, and usually follows injuries, par- 
ticularly thorn- wounds. In rare cases the hands or other parts 
are affected. At first there is nodular inflammatory swelling, be- 
ginning on the plantar surface or dorsum of the foot and spread- 
ins; to the sides. These swellings 

o — 

are hard and painless. Later, fs&r-~ 

softening occurs and rupture \f 

takes place. Thin, watery pus \ \ ^-.pV'. -*•'-. ] 

is discharged, and this contains ^ » > \\ ' " *}; ■ i * 

grayish or reddish granular bod- r - ' '- r 

ies or black granules resembling . J . / ; - 

particles of gunpowder. In the }$v/'K-': ' ■ t - 

former case the term pale myce- • ' ; ; A 

toma is applied ; the latter vari- I ■ 

ety is called black or melanoid. ' ,-v' ,' ■ ' J'* V 

In the later stages of the disease f ) v '•>'; {>. V^'^ V '" 

discharging sinuses may remain, j '^v^ 5 » ; - T" \ * V K 

while newer nodules in turn are I >V a / 

formed and soften. Finally, the 

member affected becomes greatly ^k&i'$??\^~ ' 

deformed, the portions not in- 

volved growing thin, while the ' v 

diseased part increases in size. i . 

Death occurs from exhaustion or i. M 

complications. j > 

Histologically the nodules re- ! * , ■ '' 

semble large tubercles, but are | ^ • 7 ^ V" I 

highly vascular. _ The bulk of J^^^^k^ 

the growth consists OI granula- tion of diseased tissue (Vincent). 

tion-tissue cells, those in the cen- 
ter being small, those near the outer edge often large and contain- 
ing two or more nuclei. True giant-cells are rare. In the center 
may be found a branching micro-organism, called Streptothrix Ma- 



262 



TEXT-BOOK OF PATHOLOGY. 



durce (Vincent). This stains by Gram's method, and sometimes 
shows somewhat bulbous swelling of the ends of the threads and 
their branches (Fig. 101). Around the organism may be seen an 
area of degeneration, having a striate arrangement suggesting that 
seen in actinomycosis. Extensive degeneration and pus-formation 
occur in the center of the diseased areas in the later stages ; and 
hemorrhage may occur from the new blood-vessels. Histologic 
examination of the granules in the pus shows the micro-organisms 
in the form of interlacing threads. Bodies resembling spores have 
occasionally been described. 

The organism has not as yet been definitely classified. It is 
certainly allied with the actinomyces, but probably not identical. 
It has been cultivated upon various media, particularly infusions 
of hay and the like, rendered slightly acid in reaction. It forms 
small nodular and hard growths, which become rose-red in color 
when they cling to the sides of the test-tube near the surface of 
the liquid, or brownish when they sink to the bottom. Upon 
agar isolated grayish or later rose-red clusters are formed. In- 
oculation-experiments have thus far met with little success. 
Local reaction has been so produced, but not a definite disease. 

Other Streptothrices. — Several other less important forms of the group 
streptothrix have been described, as, for example, the variety found by 
Eppinger in abscess of the brain, and those discovered by Flexner and by 
Buchholtz in pseudotuberculosis of the lung. These forms have not as yet 
received definite classification. In this connection it is interesting to note 
that the tubercle bacillus under certain conditions assumes forms suggest- 
ing a close relationship with the streptothrices, and that a bacillus has been 
found upon hay and various vegetables, and in the feces of animals, that 
caused typical tubercles when injected into animals in pure culture. 



RELAPSING FEVER. 

Definition. — Relapsing fever, or typhus recurrens, is an in- 
fectious and contagious disease, probably caused by a specific organ- 
ism which is found in the blood. 

Btiology. — The Spirochseta Ober- 
meieri is a spiral organism, in length 
several times the width of the red cor- 
puscle (16 to 40 //). It is found in the 
fresh blood, and presents active move- 
ments due to flagella (Fig. 102). The 
organism stains well with ordinary 
anilin dyes. The relation of this spi- 
rillum to the disease can hardly be 
questioned, as it is invariably present 
fig., 102 -spirochaeta obermeieri an d appears in the blood during; the 

m the blood (von Jaksch). ±r & 

paroxysms ot lever and disappears in 
the intervals, thus showing its relation to the symptoms of the 




BACTERIA AND DISEASES DUE TO BACTERIA. 263 



disease. The organism has not as yet been cultivated, but by 
inoculation with blood a number of investigators have transferred 
the disease to monkeys and human beings. 

Pathologic Anatomy. — The spleen becomes greatly en- 
larged ; it frequently presents a variegated appearance on section, 
due to areas of anemic infarction and necrosis or fatty degenera- 
tion alternating with deeply congested portions. 

Pathologic Physiology. — The peculiar feature of relapsing 
fever and the one that has given it its name is the recurring par- 
oxysms of fever. The cause of this periodicity is as yet unknown, 
though it is likely that the development of the spirochseta is such 
as to determine the relapses. 

INFLUENZA. 

Definition. — Influenza is an infectious disease occurring in 
widespread epidemics and caused by a specific bacillus. 

Etiology. — The Bacillus influenzae was discovered by Pfeif- 
fer and Canon in 1892. The bacilli are extremely small and 
usually occur singly, though they are occasionally united by the 
ends, forming short chains. They may be stained with the ordi- 
nary anilin dyes, especially with carbol-fuchsin, but are decolorized 
by Gram's method. The ends of the bacillus are somewhat swol- 
len and usually stain rather more deeply than the shaft. This 
gives the organism somewhat the appearance of a diplococcus or 
dumbbell-shaped bacillus. It is not motile. It has been culti- 
vated upon glycerin-agar and upon blood-serum, forming minute 
drop-like colonies, seen with difficulty with the naked eye, but 
clearly with the aid of a lens. The colonies do not coalesce. The 
appearance of the growth is somewhat like that of condensed 
moisture on the surface of the culture-medium. 

The bacilli occur abundantly in the sputum of the disease, de- 
creasing in quantity as the case advances. When purulent expec- 
toration ceases the bacillus disappears entirely. In fatal cases it 
has been found in abundance in the tissues of the lung, particu- 
larly in cases in which complicating pneumonia has existed. It 
does not occur in other diseases. Animal experimentation has thus 
far been unsatisfactory, though the organism has proved patho- 
genic for certain animals. Definite results have not, however, 
been reached, and the specific character of the organism is inferred 
rather than demonstrated. 

Pathologic Anatomy. — There are no specific lesions in this 
disease. The organisms provoke intense catarrhal processes and 
doubtless at times pneumonia. In some cases the pneumonia of 
grip is caused by mixed or secondary infection. 

Pathologic Physiology. — Very little is known regarding 
the mode of activity of the bacteria. The constitutional symp- 



264 



TEXT-BOOK OF PATHOLOGY. 



toms suggest toxemia, but the nature of the poison is obscure. 
The immunity from the disease must be exceedingly short, as re- 
curring attacks and relapses may be frequent and succeed one 
another rapidly. Certain complications and sequels, such as in- 
flammations of the serous surfaces and neuritis, indicate general- 
ized infection and intoxication. 



BUBONIC PLAQUE. 

Definition. — The bubonic plague, or pest, is an infectious 
disease due to a peculiar bacillus. 

Etiology. — The bacillus of bubonic plague was discovered 
by Yersin and Kitasato independently in 1894. In blood drawn 
from a puncture of the skin and in pus from the affected glands 
may be found small bacilli somewhat resembling the influenza- 
bacillus. These organisms may be stained readily, and are then 
seen to be swollen somewhat at the ends and more deeply stained 
at the poles than in the center (Fig. 103). This gives them an 



Fig. 103.— Bacillus of bubonic plague (Yersin). 

appearance resembling that of the diplococci, and in specimens 
from the blood or tissues there is an indistinct capsule. The 
bacillus is feebly motile, but flagella have not been detected. 
Pure cultures have been obtained upon various media. Upon 
glycerin-agar moist, rounded, whitish or bluish-white colonies are 
formed. Portions of such colonies removed for examination show 
the bacilli ranged in chains. 

Pathogenicity. — The bacillus has been found pathogenic for 
mice, rats, guinea-pigs, and rabbits, and the symptoms produced 
by pure cultures are the same as those induced by inoculating ani- 
mals with blood or portions of tissue from diseased persons. The 
lymphatic glands may be swollen and petechial hemorrhage may 
occur as in the human disease. 



BACTERIA AND DISEASES DUE TO BACTERIA. 265 



Inoculation in man is most frequently caused by injuries of 
the skin, such as scratch-marks, etc. Infection may, however, 
occur through the lungs. 

Distribution. — In the human being suffering from bubonic 
plague the bacilli are found in the local lesions of the lymphatic 
glands, the buboes ; and also in the blood and various organs. 
Rats and mice frequently die during epidemics, and doubtless help 
to spread the disease by infecting the soil and dust about dwell- 
ings. Yersin showed that flies die of the disease, and succeeded 
in obtaining the bacillus from their dead bodies. 

Pathologic Anatomy. — The organism produces swellings 
and suppuration of lymphatic glands, particularly those of the 
groin, and secondarily lesions of internal organs. The lymphatic 
glands swell quickly, become tender and congested, and then 
soften, forming a rather thick pus. -This is sometimes somewhat 
blood-tinged. Petechial hemorrhages and blood-stained effusions 
into the serous cavities may occur. Petechias of the skin are apt 
to develop as a result of slight traumatisms. Thus the bite of an 
insect, instead of producing its usual results, may cause distinct 
ecchymoses in persons suffering from the disease. A form of 
bronchopneumonia occurs in a considerable proportion of cases. 
In these the primary infection may be caused by the inhalation 
of dust. 

Pathologic Physiology. — It seems that the distribution of 
the bacillus in the blood, as well as toxic substances, contributes 
to the general disturbance of health. By successive inoculation 
immunity has been produced, and toxins and antitoxins have beera 
obtained from the serum. The importance of these latter, how- 
ever, is still under investigation. 

THRUSH. 

This condition occurs in new-born infants and in older children 
or adults who have become weakened by disease. The organism 
called O'idium albicans is a budding fungus, though some believe 
it a form of mould. If some of the milk deposits on the mu- 
cous membrane of the mouth which characterize the disease be 
removed and examined microscopically, mycelia-threads and 
conidia are observed. The organism may be cultivated upon 
gelatin plates, in the form of whitish colonies on the surface, or 
granules with radiating processes in the depth of the medium. 
On potato and on bread it forms a white coating. The organism 
is present in the air and in various articles of food, so that infec- 
tion readily takes place. 

PHARYNGOMYCOS1S LEPTOTHRICIA. 

The Leptothrix buccalis is a normal inhabitant of the mouth, 
and occasionally produces a pathologic lesion of clinical interest, 



266 



TEXT-BOOK OF PATHOLOGY. 



The organism probably belongs to the group of pleomorphic bac- 
teria, though its exact position is not determined. It consists of 
fine threads, of wavy or spiral character, composed of rod-like 
segments. Occasionally, spore-like bodies are found at the free 
ends of the filaments. The organism sometimes penetrates and 
multiplies in the crypts of the pharynx, causing a chalk-like 
nodule or deposit. Secondary inflammation may be occasioned. 
(See also Diseases of the Pharynx.) 

DISEASES OF UNCERTAIN BACTERIOLOGY. 
SYPHILIS. 

Definition. — Syphilis is a specific contagious disease of man, 
of uncertain etiology. The disease has never been observed in 
any of the lower animals. 

Etiology. — The attempts to find a specific cause of this dis- 
ease have not as yet met with definite success. The organism 
which at the present time has the best claim to recognition is that 
observed by Lustgarten. This resembles the tubercle-bacillus 
very closely. It is 3 to 7 p. long, and often somewhat curved and 
swollen at the ends. It stains with difficulty, and a complicated 
method was suggested by the discoverer. The bacilli are found 
in the diseased areas in small numbers, lying within the cells and 
partly between them. It has also been claimed that they occur in 
the blood. The organism has never been isolated or cultivated 
upon artificial media. Furthermore, it is difficult to distinguish 
this supposed specific germ from other bacilli, notably the smegma- 
bacillus, by the staining-methods suggested. 

Whatever the nature of the organism, it is quite certain that 
the disease is definitely infective. In the great majority of cases 
infection occurs by direct inoculation in sexual intercourse. It 
may, however, be conveyed in many other ways. Physicians are 
sometimes infected in performing surgical operations or in exam- 
ining syphilitic cases ; persons have frequently been inoculated in 
the process of tattooing or vaccination when saliva or vaccine- 
lymph from diseased individuals was employed. Infection may 
be caused by kissing, or indirectly by the use of drinking-vessels 
which have been employed by the diseased. The new-born may 
be syphilitic in consequence of disease of the father or mother ; and 
healthy wet-nurses may be infected by syphilitic nurslings. In 
addition to the specific cause, surrounding conditions and individ- 
ual susceptibility doubtless play a part. During the Middle Ages 
this disease at times and in certain places almost attained the char- 
acter of a universal scourge. Its manifestations were severe, its 
course rapid, and in every sense its nature was malignant. Cases 
of this description are exceedingly rare at the present day. 



BACTERIA AND DISEASES DUE TO BACTERIA. 267 



Pathologic Anatomy. — The pathologic course of this dis- 
ease may be divided into three stages : the initial stage, the second- 
ary stage, and the tertiary stage. 

Chancre. — In the initial stage there is formed at the point of 
inoculation a primary lesion, commonly termed chancre. This 
may make its appearance first as a somewhat red and inflamed 
papule, or as a vesicle which ruptures and thus produces an ero- 
sion. When it begins as a papule the surface soon becomes eroded, 
and thus a superficial ulceration is established. The peculiar feat- 
ure of this lesion, to which Hunter called particular attention, is 
its hardness or induration, and it is by this feature largely that it 
is distinguished from the soft chancre or chancroid. The initial 
or primary lesion may remain indolent or as a small erosion for a 
long time, or it may soon cicatrize and leave a more or less definite 
scar. The chancre occurs upon the glans penis or prepuce, or 
within the urethra of the male ; and in the vagina, urethra, or upon 
the cervix uteri and external genitalia of the female. Extrageni- 
tal chancres may be observed in the rectum or anus, on the lips 
or tongue, tonsils or pharynx, the fingers, or other parts. 

Secondary Lesions. — At the end of a variable period of time 
after the eruption of the initial sore secondary manifestations of 
the disease make their appearance. The first among these, as a 
rule, are swelling and induration of the neighboring lymphatic 
glands (syphilitic bubo). Later the superficial lymph-glands of 
the entire body become swollen and, like those in the neighbor- 
hood of the lesion, indurated. At the same time eruptions upon 
the skin and mucous membranes make their appearance. The 
interval between the primary and the secondary manifestations is 
variable. Sometimes it is but a few weeks (three or four), at other 
times it may be several months. The manifestations of the sec- 
ondary stage may begin with fever and constitutional symptoms, 
suggesting sudden and recent infection, and at the same time 
changes in the blood (rapid reduction of red corpuscles, moderate 
leukocytosis) make their appearance. Among the lesions of the 
skin various forms of papules, macules, and scaly eruptions are 
most frequent and characteristic. The lesions are usually sym- 
metrically arranged on the two sides of the body and cause but 
little irritation. The color of the skin is frequently said to be 
somewhat coppery. On the mucous membranes and neighboring 
skin the most characteristic lesion of this stage is the condyloma 
latum, or mucous patch. This appears as a somewhat elevated 
patch with superficial erosion or ulceration. The surface has a ne- 
crotic appearance, and may be covered with more or less secretion. 

Tertiary Lesions. — These may take the form of ordinary in- 
flammatory changes of the mucous membranes or of other parts, 
with a pronounced tendency to fibrous-tissue overgrowth and 
thickening, or of definite nodules — the syphilitic gummata, or 



268 



TEXT-BOOK OF PATHOLOGY. 



syphilomata. Among the diffuse syphilitic changes of the tertiary 
stage may be ranked atheromatous thickening of the intima of the 
blood-vessels, certain changes in the liver, spleen, kidneys, and 
heart-muscle, and doubtless also similar alterations in the nervous 
system. 

The localized lesions of the tertiary stage — the gummata — are 
most frequent in the bones (tibia, sternum, and skull) ; and in the 
internal organs, such as the liver, lungs, kidneys, heart, and brain. 

The gumma presents itself as a nodular mass, varying in size 
from small tubercle-like formations (miliary gummata) to tumors 
the size of an orange, or larger (Fig. 104). It is hard, and has 



Fig. 104— Gummata of the liver. 

frequently an elastic character, which has suggested the name 
gummy tumor or gumma. On section the substance is frequently 
found to be gelatinous or mucoid in appearance; but there is 
nearly always considerable induration, either peripheral, in the 
form of a capsular enclosure, or striate, in the form of bands 
extending from the center to the periphery and into the sur- 
rounding tissue. Occasionally gummata soften very rapidly and 
become converted more or less completely into puriform collections. 
When situated in the mucous membranes or adjacent to the sur- 
faces of the body, suppurative, fatty or necrotic softening may 
lead to the formation of superficial ulcerations. These may re- 
main indolent, or may gradually become cicatrized. Sometimes a 
gummatous lesion disappears entirely by absorption without leav- 
ing a trace of its existence. 

Histology. — In syphilitic processes of all kinds and in all of 
the stages there is a tendency to accumulation of the round cells 
and proliferation of connective-tissue cells, the processes being 
first manifest around the smaller blood-vessels, but subsequently 



BACTERIA AND DISEASES DUE TO BACTERIA. 269 



extending to other parts of the tissue. The walls of the blood- 
vessels themselves are frequently involved, and thickening of the 
inner or of all the coats may be observed. Complete destruction 
of the vascular channels is not rarely the consequence. In the 
subsequent course of the disease there is a tendency to the forma- 
tion of distinct cicatricial connective tissue, giving rise to indurated 
scars or diffuse sclerosis ; and a less pronounced tendency to the 
occurrence of degenerations, mucoid and fatty, causing areas of 
degenerative softening. 

The Chancre. — The initial lesion first presents small areas of 
round-cell infiltration in the deeper layers of the skin or mucous 
membrane, and as a rule in the neighborhood of the blood-vessels. 
The connective tissue at the same time undergoes proliferative 
change, and spindle-shaped cells or irregular embryonal connec- 
tive-tissue cells are found mingled with the round lymphoid cells, 
or surrounding the foci of the latter. Thickening of the blood- 
vessels may be observed in the later stages or from the very first. 
The tissue-elements of the skin and of the subcutaneous tissue are 
usually separated by infiltrating liquid, and the latter may loosen 
the tissues of the surface and cause exfoliation of the superficial 
epidermis, and thus lead to the development of the primary vesicle 
or the erosion so commonly seen. The induration of the chancre 
is probably the result of the sclerosis of the vessels and the gen- 
eral connective-tissue hyperplasia, as well as in part due to the 
tense infiltration of serous liquid. 

The Mucous Patch. — The condyloma latum is very similar in 
structure to the initial lesion. There is, first, round-cell infiltra- 
tion of the deeper layers of the mucous membrane, with serous 
exudation and erosion of the surface. Later, there is a tendency 
to connective-tissue hyperplasia, though this is less marked than 
in the case of the chancre. 

The Tertiary Lesions. — The gumma is composed in large part 
of round cells derived from the blood-vessels and proliferated 
connective-tissue cells having a spindle-shape or various irreg- 
ular forms. Epithelioid cells are less abundant, and giant-cells, 
though occurring at times, are usually few in number. The 
blood-vessels are nearly always more or less affected, the intima 
particularly being thickened ; there is also new formation of blood- 
vessels, the lesion in this respect differing from the nodular lesion 
of tuberculosis (Fig. 105). Secondary changes are almost always 
seen in gummata of considerable dimensions. Among these may 
be recognized a gradual necrotic transformation of the cells in the 
center of the lesion, with distinct fatty degeneration or myxoma- 
tous change. The degenerated tissue may be infiltrated by leuko- 
cytes in a state of fair preservation. 

In the diffuse tertiary lesions of syphilis the tissues of the 
affected organ are indurated, the connective tissue showing more 



270 



TEXT-BOOK OF PATHOLOGY. 



or less pronounced hyperplasia. These processes cannot be 
certainly distinguished by their microscopic or general features 
from sclerosis due to other causes. 

Pathologic Physiology. — Syphilis is one of the most per- 
sistent of the infectious diseases, and occasions widespread changes 
that are doubtless toxic in character. The nature of the toxic 




Fig. 105. — Gummatous meningoencephalitis (Ziegler). 



principles, however, is entirely unknown. In the tertiary stage 
pronounced anemia (cachexia) is frequent; and in the secondary 
stage rapid chloro-anemia with leukocytosis is quite common. 



Congenital Syphilis. 

Syphilitic lesions may be found in the new-born, or may 
develop some time after birth. Not rarely they occur in the new- 
born fetus, and cause its premature death. Frequently there is 
maceration of the fetus prior to expulsion. Among the lesions 
observed, sclerotic changes in the lungs, liver, spleen, pancreas, 
and other organs are conspicuous ; and a certain condition of the 
bones is quite characteristic. The latter consists of a hyperplasia 
of connective tissue and fatty degeneration at the junction of the 

epiphyses of the long bones with the 
shafts. Various superficial lesions of 
the skin in the form of vesicles or 
bullae, fissure, and the like may be 
observed. The blood may present 
considerable excess in the number 
of leukocytes. An almost distinctive condition of second denti- 
tion is that known as Hutchinson's teeth. This consists of a 
notched indentation of the cutting surface of the upper central 




Fig. 106.— Hutchinson's teeth. 



BACTERIA AND DISEASES DUE TO BACTERIA. 271 



incisors. In addition, the teeth are often wedge-shaped and peg- 
like (Fig. 106). All cases of inherited syphilis do not present this 
condition, and it occasionally occurs in non-syphilitic children. 

SOFT CHANCRE. 

Definition. — The soft chancre or chancroid is an infectious 
venereal sore appearing upon the external genitalia. The bacil- 
lus of Ducrey may be the specific organism. 

Etiology. — The soft chancre occurs almost exclusively upon 
the genital organs or the surrounding parts. It is always caused 
by direct contagion. 

The bacillus of Ducrey and Unna is a rod-shaped organism 
about 1.8 jul in length and 0.5 /i in thickness, and is somewhat 
compressed in the middle, so that it has a figure-of-8 shape. The 
ends are rounded and the organisms often occur in chains, or later 
in the disease in pairs as a diplobacillus. 

The demonstration of the bacillus in the pus is comparatively 
easy. The specimen is stained with alkaline solutions of methyl- 
ene-blue and quickly decolorized with weak acetic-acid solution. 
In the tissues the demonstration is more difficult. 

The cultivation of the bacillus has not thus far proved success- 
ful, though certain bacteriologists claim they have succeeded. 

The bacillus is found in the pus of the soft chancre, as well as 
in the deeper parts, lying between the cells and frequently within 
the leukocytes. It has also been discovered in the pus and walls 
of ulcerating buboes, but is generally absent in the pus of un- 
opened buboes. 

Mixed Infection. — Various other organisms have been found 
associated with the bacillus, including streptococci, staphylococci, 
the gonococcus, and bacilli of uncertain nature. 

Pathologic Anatomy. — The soft chancre is an ulcer of 
variable character. Usually it is a simple ulcer, with suppurating 
base and edges, not differing from ulcers due to other causes. 
Sometimes the ulceration seems more malignant and takes on a 
phagedenic or serpiginous character (see Ulceration). The neigh- 
boring lymphatic glands are usually enlarged and sometimes 
undergo suppurative softening (bubo). 

Pathologic Physiology. — Little is known of the existence 
of special toxic bodies in this disease. It is believed, however, 
by some that toxins are produced by the bacilli, and that these are 
capable of producing secondary lesions (bubo) without the presence 
of the bacilli themselves. 

YELLOW FEVER. 

Definition. — Yellow fever, or typhus icteroides, is now recog- 
nized as infectious and contagious, and it is probably caused by a 
specific bacillus recently isolated. 



272 



TEXT-BOOK OF PATHOLOGY. 



Etiology. — The Bacillus icteroides was discovered in 1897 by 
Sanarelli. This is a small bacillus from 2 to 4 p. in length, with 
rounded extremities. It is frequently united in pairs, and is actively 
motile, the motility being due to from four to eight lateral flagella. 
The organism is pleomorphous. It is readily stained by the ordi- 
nary anilin dyes, but is decolorized by Gram's method. 

Cultivation. — Sanarelli succeeded in obtaining cultures upon 
the ordinary media, but the growth on the surface of agar is most 
distinctive. When incubated for twelve hours at 37° C. (98.6° F.) 
and then allowed to develop further at lower temperatures there 
will be found, first, semitransparent rounded colonies, and, later, 
enlargement of these with the formation of a thick white border, 
giving the appearance of a drop of sealing-wax. The character- 
istic growth is thus obtained in twenty-four hours. 

Distribution. — Sanarelli found the bacillus in the various organs 
as well as in the blood. He succeeded in obtaining cultures in 58 
per cent, of the cases studied. Failure in a large proportion of 
cases he attributed to the small number of bacilli present. 

Pathogenicity. — The pathogenic role of this organism is becom- 
ing quite widely recognized. The discoverer succeeded in produc- 
ing in animals lesions and symptoms very analogous to those of the 
human disease. The dog responded most satisfactorily. Injected 
into the veins of a dog there is active emesis, then hemorrhages 
throughout the body, and finally extensive fatty degeneration of 
the liver and kidneys. In one case extreme jaundice developed. 

Other Micro-organisms. — Previous to Sanarelli's work a great 
variety of organisms had been described. Among others a bacil- 
lus by Richardson, a micrococcus by Finlay and Delgado, a 
bacillus by Gibier, and other organisms by Freire and Carmona 
and by Sternberg. None of these organisms appears to have im- 
portance, or to be the same as that discovered by Sanarelli. The 
organisms isolated by Havelberg about the same time as SanarellPs 
appear to be of no importance. 

Pathologic Anatomy. — The lesions of this disease are 
mainly those of the internal organs — liver and kidneys. In the 
liver extensive fatty degeneration leads to some swelling and light 
color of the organ, and on section there may be mottled appear- 
ance due to the alternation of healthy and fatty areas. In the 
kidneys degenerative changes of the parenchyma and extravasation 
of blood are associated in varying proportions. The appearance 
may be that of an acute hemorrhagic nephritis, or more particu- 
larly that of degenerative nephritis. Hemorrhages in the mucous 
and serous surfaces are frequent, particularly extravasation of the 
mucosa of the stomach. 

Pathologic Physiology. — The organism of yellow fever 
probably produces abundant toxin. Small numbers of the bacilli 



BACTERIA AND DISEASES DUE TO BACTERIA. 273 



seem at times to give rise to violent symptoms. Sanarelli has 
claimed that antitoxic serum is obtainable from immunized 
animals. Kecently an agglutinative reaction, like that of Widal 
for the typhoid germ, has been described. 

MEASLES. 

Measles, or rubeola, is an infectious and contagious disease in 
all probability due to some micro-organism. A number of micro- 
organisms have been discovered. Several observers (Canon and 
Pielicke, Czajkewski) have found a bacillus somewhat resembling 
that of influenza ; others have found bacilli resembling the pseudo- 
diphtheria bacillus, but the bacteriology is still unsettled. Doehle 
described a protozoan organism occurring in the blood. 

SCARLET FEVER. 

Scarlet fever, or scarlatina, is an infectious and contagious 
disease probably due to a micro-organism. A variety of organ- 
isms have been discovered in cases of scarlet fever, but none as 
yet has proved to be specific. The weight of evidence seems to 
suggest the pyogenic micrococci (streptococci) as probable etiologic 
agents. This, however, is by no means established. Protozoan 
organisms have also been described (Doehle). 

MUMPS. 

The bacteriology of mumps is uncertain. Charrin and Capitan 
isolated a number of organisms, mainly micrococci and motile 
bacilli. A number of other authors subsequently obtained simi- 
larly indefinite results. Laveran and Catrin in 1893 found a 
diplococcus. 

WHOOPING=COUGH. 

A short bacillus was discovered in the expectoration of pertus- 
sis by Afanassiew in 1887. He injected cultures of this into the 
trachea and lungs of dogs, and found that the animals became ill 
and died, after presenting convulsive cough with bronchitis similar 
to that of whooping-cough. Wendt confirmed these results ; but 
Bitter found a diplococcus in his cases, and Cohn and Neumann 
found small cocci, often arranged as diplococci or more rarely as 
short chains. Czaplewski and Hensel describe a bacillus resem- 
bling the xerosis bacillus, and believe that the organisms of 
Cohn and Neumann were identical with theirs. Others have dis- 
covered organisms similar to the ordinary pyogenic micrococci ; 
and some have described protozoa in the blood. 

18 



274 



TEXT- BO OK OF PATHOLOGY. 



TYPHUS FEVER. 

A number of micro-organisms have been discovered in this 
disease, including strepto-bacilli (Hlava), small granular bodies 
growing to thread-like organisms (Thoinot and Calmette ; Lewa- 
scheff), diplococci (Dubief and Bruhl). Lewascheff has more 
recently concluded from a study of 158 cases that the micrococci 
of Dubief and Briihl, which have also been described by others, 
are the important agents, and proposes the name Micrococcus exan- 
thematicus. 

RABIES. 

Hydrophobia is doubtless an infectious malady, but the bac- 
teriology is still obscure. Micrococci and bacilli of different 
kinds have been described. Memmo isolated a form of blasto- 
mycetes, and claims to have produced the disease in dogs with 
pure cultures of this. 

PROTEUS INFECTION. 

The Bacillus proteus vulgaris and its several sub-varieties occur in decom- 
posing animal matter and in association with necrotic and gangrenous pro- 
cesses in the living body. The organism is a small, motile bacillus, occur- 
ing in pairs and less often in chain formations. It is abundantly sup- 
plied with flagella. 

Cultivation and Demonstration. — The organism grows very well at 
ordinary temperatures, and forms characteristic growths on gelatin plates. 
At first yellowish colonies with outgrowths are formed ; the gelatin lique- 
fies, and the outgrowths move about in a tortuous manner and become sepa- 
rated from the original growth. Peculiar figures are formed, and the term 
Bacillus figurans has been applied. The cultures have a putrid odor. The 
organism is readily stained with ordinary solutions like carbol-fuchsin. 

Pathogenicity. — Injected intravenously in animals, hemorrhagic vomit- 
ing and diarrhea result. In man the bacillus has been found associated 
with phlegmonous inflammations, gangrenous processes, cystitis, and in 
infectious icterus (Weil's disease). 

THE HEMORRHAGIC DISEASES. 

The hemorrhagic diseases constitute a group of affections of 
probably quite divergent character, which, however, are similar 
in presenting hemorrhages in and from the mucous membranes, in 
the skin, serous surfaces, and in the deeper tissues or organs. 

The general causes of hemorrhage must be considered in con- 
nection with these diseases. Among the causes capable of pro- 
ducing hemorrhages such as occur in the hemorrhagic diseases are 
mechanical conditions , as atheroma or other diseases of the walls 
of the blood-vessels ; toxic conditions, such as poisoning by the 
venom of animals and by various blood-poisons, and probably 
obscure poisons produced in the course of anemic or other dis- 
eases ; infectious conditions, such as occur in hemorrhagic variola, 



BACTERIA AND DISEASES DUE TO BACTERIA. 



275 



scarlatina, etc. ; and nervous conditions, as are illustrated in the 
hemorrhages following injuries to the brain and those accompany- 
ing certain states of cerebral excitation. 

Clinically the hemorrhagic diseases or purpuras may be classi- 
fied as primary and secondary, the former occurring without any 
definite preceding disease ; the latter being symptomatic of various 
disorders. Among the primary there are: (1) infectious for ins, 
including, with more or less probability, purpura, scurvy, and 
various forms of cryptogenetic sepsis ; (2) toxic forms, as those due 
to drugs and venom of animals ; (3) mechanical forms, as hemo- 
philia. Among the secondary purpuras are : (1) infectious forms, 
as scarlatina, variola, and the like ; (2) mechanical forms, as those 
due to cardiac and arterial diseases, or embolism ; (3) toxic forms, 
as those resulting from intestinal auto-intoxications, jaundice, 
pernicious anemia, etc. ; and (4) nervous forms, as those due to 
hysteria, diseases of the brain, etc. 

The infectious purpuras interest us particularly in the present 
place. Various micro-organisms have been found in different 
forms of hemorrhagic disease. Kolb described a bacillus patho- 
genic for animals, which occurred in five cases of hemorrhagic 
purpura. Babes and Oprescu isolated a bacillus from one case of 
hemorrhagic septicemia, and others have found various micrococci, 
especially the streptococcus. It is not unlikely that many of the 
micro-organisms may assume a peculiar virulence and acquire the 
power to produce hemorrhages under certain circumstances. 

In scurvy several micro-organisms have been described, but 
the one which has the best claim for consideration is that discov- 
ered by Babes, a delicate bacillus occurring in the gums. Strepto- 
cocci were found in association with it. 

RHEUMATISM. 

Definition. — Acute articular rheumatism is probably an in- 
fectious condition ; the nature of the infectious agent, however, is 
uncertain. 

Etiology. — The manifestations of rheumatism agree very well 
with those of infectious diseases, and some of the lesions frequently 
complicating the disease, such as endocarditis, are invariably in- 
fective. The relationship between tonsillitis and rheumatism has 
been explained by some as that between primary and secondary dis- 
order. It is supposed that the infectious agents effect an entrance 
into the body through the tonsils, causing primary tonsillitis and 
secondary general infection, with localization in the joints. In 
other cases it has been held that the organisms enter through 
abrasions of the skin or in other ways. 

Guttmann, one of the first to maintain the infectious origin, 
described a Staphylococcus pvogenes flavus discovered in one of 



276 



TEXT-BOOK OF PATHOLOGY. 



his cases. Sahli found an organism which he classified as Staphylo- 
coccus pyogenes citreus. He enunciated the theory that rheuma- 
tism represents a form of staphylococcic infection, the organisms, 
however, being of a low grade of virulence. They are not found 
abundantly in the exudations in the joints, as they remain fixed in 
the synovial tissues. Hence, they are difficult of discovery. 
Other organisms, including various forms of bacilli, have been 
described. 

Very recently Achalme has described a bacillus which he and 
others have found in a number of cases of acute articular rheuma- 
tism. It is a large bacillus resembling that of anthrax ; sometimes 
it is motile ; it stains well with anilin dyes and with Gram's stain • 
may have a capsule ; and forms polar spores much larger than the 
bacillus. This organism is obligate-anaerobic, growing best in 
liquid media, in which it forms small bubbles of gas. Thioroloix 
claims to have produced typical symptoms in the rabbit ; and the 
inoculation-experiments of others have given suggestive results. 
This bacillus was obtained from the blood in a number of cases ; 
and from the pericardial fluid and blood in a state of purity in one 
case. The organisms have been found in sections of the heart- 
muscle and valves. 

[For the pathologic anatomy of rheumatism, see Diseases of 
the Joints.] 

MALTA FEVER. 

Synonyms. — Mediterranean Fever ; Gibraltar Fever ; Febris 
Undulans. 

Definition. — This disease has been described as a form of 
irregular fever occurring along the Mediterranean coasts. It 
has been regarded as an aberrant form of typhoid fever, but is 
probably independent and due to a special micro-organism. 

Htiology. — The micro-organism discovered by Bruce, and 
designated Micrococcus Maltensis, is by many regarded as the 
specific cause. This is an oval micrococcus about ^ fi in diameter, 
occurring singly or sometimes in pairs, but never in chains. It 
has no motility of its own. It may be stained with ordinary solu- 
tions of anilin dyes, but not by Gram's method. It occurs abun- 
dantly in the spleen, but not in the blood. Pure cultures have 
been obtained, and inoculation in monkeys has seemed to give 
positive results. Malta fever is not contagious. The micro- 
organisms seem to enter the body through the respiratory or the 
intestinal tract. 

Pathologic Anatomy. — The mucous membrane of the small 
intestine is red and the solitary follicles and Peyer's patches are 
sometimes swollen. The mucosa of the large intestine is generally 
dark red and presents small round or larger irregular ulcerations, 
from which intestinal hemorrhages occur. In some cases lesions 
of the ileum resembling those of typhoid fever have been de- 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 277 



scribed ; but it is doubtful if the cases in which these occurred 
were Malta fever, and not typhoid. The spleen is enlarged and 
hyperemic. 

Pathologic Physiology. — Malta fever is characterized by 
irregular febrile movements. The cause of this irregularity and 
the nature of the toxic substance generated in the disease are un- 
known. Recently a serum-reaction, like that of Widal for typhoid 
fever, has been obtained with the serum and cultures of Malta 
fever. 

BERI=BERI. 

Definition. — This disease is an infection due to undetermined 
causes. It occurs in tropical and subtropical countries, and is 
characterized by muscular weakness, generalized muscle-pains, 
dropsy, and cardiac failure. The essential lesions seem to be 
degeneration and inflammation of the peripheral nerves. 

Etiology. — Beri-beri occurs among young persons and usually 
affects numbers of people. It is most frequent along ocean coasts 
and great rivers, and is most prevalent during damp seasons of 
the year. It does not seem to be contagious. 

Various micro-organisms have been described, including a 
number of bacilli and micrococci, as well as organisms resembling 
the malarial hematozoa. One observer (Taylor) was able to 
produce the disease in animals by the injection of blood from a 
diseased person. 

Pathologic Anatomy. — Among the ■ lesions observed are 
punctate hemorrhages in the serous surfaces ; parenchymatous and 
fatty degeneration of the heart-muscle ; enlargement of the liver 
and spleen. Degeneration and inflammation of the peripheral 
nerves are constant and important conditions. 



CHAPTER VIII. 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 

PROTOZOA. 

Classification. — The protozoa, according to Butschli, may be divided into 
four classes : 1. Sarhodina, forms having the general characteristics of 
amoebse ; 2. Mastigophora (flagellata), forms having a small number of 
flagella ; 3. Infusoria (ciliata), forms which have a more elaborate arrange- 
ment of cilia or flagella ; 4. Sporozoa, invariably parasitic protozoa which 
are rarely ameboid and multiply by a form of sporulation. These classes 
cannot be readily separated. 



278 



TEXT-BOOK OF PATHOLOGY. 



AMCEBA COLI. 

Description. — This organism, first accurately described by 
Losch, is an ameboid body from 20 to 30 fi in diameter, consist- 
ing of a clear protoplasmic outer portion and a finely or coarsely 
granular protoplasm within (Fig. 107). It frequently shows vacu- 
oles and sometimes a nucleus. It presents active ameboid move- 
ments when studied on a warm stage of the microscope ; and fre- 
quently contains foreign bodies, such as bacteria, pigment-particles, 
and portions of blood-corpuscles or other cells. 

In the movements of the organism pseudopodia are projected 
from some part of the periphery. These at first draw upon the 
clear peripheral zone, but after their formation the granuloplasm 
flows into the projected pseudopods. When in unfavorable sur- 
roundings the organism undergoes a form of change called the 
encysted state. In this the body becomes spherical, and the wall 
is eventually stiff and firm and usually presents a double contour. 



* 




Fig. 107.— Amoeba coli in intestinal mucus, with blood-corpuscles and bacteria (Losch). 

The division into a clear and a granular protoplasm is lost, the 
organism being uniformly granular. 

Distribution and Pathogenesis. — The organism in ques- 
tion has been found abundantly in the stools of patients suffering 
from dysentery. It is readily detected in the necrotic particles or 
the mucus of the stools, and has also been found in the tissues of 
the bowel-Avail adjacent to the dysenteric ulcers and abundantly in 
the liver-abscesses secondary to dysentery. 

It has, however, been found in the dejections from cases other 
than dysentery, and even in the stools of healthy individuals. 

The pathogenic importance of this organism cannot be positively 
established until cultures are obtainable. Thus far, attempts to 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 279 



secure pure cultures have failed. The injection of mucus contain- 
ing the amoeba into the rectum of cats and other animals has occa- 
sionally produced typical dysentery, but this does not prove the 
pathogenicity of the ameba. The regularity of the occurrence of 
the organism in certain forms of dysentery and its relations to the 
lesions are the strongest evidences in favor of its pathogenic role. 

Some investigators distinguish between Amoeba coli communis 
or mitis and A. coli dysenterici, according as the organism seems 
to be non-pathogenic or pathogenic when introduced into the 
rectum of cats. 

OTHER AMCEByE. 

Several other amoeba? of lesser importance have been discov- 
ered. Among these are the Amoeba urinalis, found in the urine in 
cases of cystitis, and several forms met with in the mouth, espe- 
cially about the teeth. 

CERCOMONAS INTESTINALIS. 

This organism is a pear-shaped body with a sharp anterior 
extremity provided with a delicate short cilium. The broader 
posterior end is provided with a long, tail-like flagellum. A 
larger and a smaller variety have been described (Fig. 108). The 

Fig. 108.— Cercomonas intestinalis : a, larger, b, smaller variety (Davaine). 

former is the variety usually found, and is from 10 to 12 p. in 
length. A minute oval aperture has been found at the anterior 
extremity. 

Significance. — The organism has been discovered in great num- 
bers in various diarrheal conditions, especially in cholera. It is 
not known to have pathogenic powers. It is not improbable that 
the organism is in reality a form of trichomonas. 

CERCOMONAS COLI HOMINIS. 

A single observation of this organism was made by May. The 
body of the parasite was not quite the size of a red corpuscle ; 
rather granular and glistening and slightly greenish. It was 
spindle-shaped, the anterior end more blunt than the posterior. 
Four cilia were found attached to this end, and upon one side of 
the organism was seen an undulating membrane. In the same 



280 



TEXT-BOOK OF PATHOLOGY. 



case smaller bodies, less developed and probably younger para- 
sites, were discovered. The patient suffered from carcinoma of 
the stomach and chronic diarrhea. 



TRICHOMONAS INTESTINALIS. 

This organism is pear-shaped; from 10 to 15 p. in length 
and 7 fi in breadth (Fig. 109). The anterior end is blunt ; the 
posterior end is prolonged into a sharp, tail-like projection. 




The body is granular and contains one or two bodies resembling 
vacuoles. Near the anterior end at one side may be seen a row 
of ten or twelve cilia, which give the organism active motility. It 
has also ameboid movements. 

Significance. — This organism has been found in cases of diar- 
rhea, but its significance is doubtful. 



TRICHOMONAS VAGINALIS. 

This form is rather smaller than the last, with an attenuated 
caudal end and a more blunt anterior portion, provided with three 
flagella ; there is a lateral undulating membrane with six or seven 
short cilia. 

Significance. — The organism has been found in cases of vagini- 
tis due to various causes, but also in the absence of evident 
disease. 



OTHER FORMS OF TRICHOMONAS. 

Sternberg has found several forms in the mouth, and especially 
about the teeth. These have been termed Trichomonas flagellata, 
Trichomonas caudata, and Trichomonas elongata. A trichomonas 
closely related to T. vaginalis has been found in gangrene of the 
lung and in putrid bronchitis. 



BALANTIDIUM COLI. 

Balantidium or Paramecium coli is a rounded body from 
7 to 10 fi in length and slightly less in breadth (Fig. 
110). It is surrounded by a coat of cilia closely set. There 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 281 



is an oral aperture at one end and an anal opening at the 
other. The substance of the parasite is granular, and con- 
tains a nucleus and two contractile vacuoles 
besides various foreign matters. Encysted 
forms with a thickened capsule have been de- 
scribed. 

Significance. — The hog is the natural host of 
this parasite. Man is probably infected through 
drinking-water or contaminated food-stuffs. It 
is found particularly in northern countries of 
Europe, and occurs in cases of diarrhea prin- 
cipally involving the large intestine. Chronic 
catarrhal inflammation and dysenteric lesions gten) m C ° U (Malm * 
have been described. The organism is prob- 
ably irritating, but whether pathogenic or not is unknown. 

MEGASTOMA ENTERICUM. 

This organism in its active state is irregularly pear-shaped, and 
presents at its broad end a cup-shaped depression situated obliquely 
at one side (Fig. 111). On the anterior edge of the depression are 






Fig. 111.— Megastoma entericum from the intestines of a mouse (Grassi and Schewiakoff). 



attached two long cilia, and at one point of the posterior lip are 
two pairs of cilia. In the base of the depression are seen two 
vesicular structures (nuclei) united by a band. The protoplasm 
is finely granular and is surrounded by a delicate capsule. When 
free the organism is capable of rather rapid motion, but in the in- 
testine it is attached to the epithelial cells by its cup-shaped 



282 



TEXT-BOOK OF PATHOLOGY. 



depression. The organism exists in this form m the duodenum 
and jejunum. In the colon or other unfavorable situations it 
forms oval encysted bodies showing the nuclei and cilia within. 

Significance. — Megastoma is a frequent parasite of the mouse, 
but has been found in the intestines of other animals, and occasion- 
ally in man. It has been found especially in chronic diarrheal 
conditions, and at times appears in the stools in immense numbers. 
No definite lesions have been found, and the pathogenicity of the 
germ is uncertain. 

HEMATOZOON MALARI/E. 

The organism which is now recognized as the cause of malaria 
is an animal organism of the protozoan group, the exact biologic 
position of which, however, remains undetermined. Most authors 
regard it as one of the sporozoa. It occupies the blood and the 
vascular channels of the various organs, deriving its nourishment, 
for the most part, directly from the blood-corpuscles. Malaria 
has been regarded as a water-borne and as an air-borne disease. 
No positive proofs have been obtained for either view. 

Direct contagion does not occur, but it has been shown that the 
blood is infectious when introduced into the circulation of a 
healthy person. The drinking of the blood does not give rise to 
the disease. Certain external conditions are favorable or necessary 
to the development of the disease, and probably are important in 
fostering the development of the organisms outside the body. These 
external conditions are moist, marshy soil, atmospheric humidity, 
and high temperature. The disease occurs in the lowlands or 
bottomlands, and very rarely in high and dry ground. Extensive 
excavations and the like may cause the appearance of the disease 
or increase it, and, on the other hand, suitable drainage may cause 
its diminution or disappearance. 

The Hemato^oon. — Three forms of malarial parasites have 
been distinguished ; and it is likely that these are three definite 
species, although some still maintain they are merely alterations 
of the same organism. 

The Parasite of Tertian Fever. — Examination of the fresh blood 
of a patient some hours after a tertian chill shows in some of the 
red corpuscles small hyaline bodies, having ameboid movement 
and often assuming cross- or star-shapes. These are the so-called 
plasmodia. Later, the plasmodia have pigment about their pe- 
riphery, and finally the amount of pigment may become consid- 
erable. During this time the organism grows and the red cor- 
puscle becomes paler. Eventually the ameba may almost com- 
pletely fill the corpuscle. At this stage, which occurs just prior 
to the paroxysm, segmentation begins. The pigment, which pre- 
viously has shown active movements, collects tow r ard the center and 




73 



14 




20 27 22 

# (i 1 

i>J 26 27 



Various forms of malarial parasites (Thayer and Hewetson) : Figs. 1 to 10, in- 
clusive, tertian organisms ; Figs. 11 to 17, inclusive, quartan organisms ; Figs. 18 to 
"27. inclusive, estivo-autumnal organisms. 

Fig. 1.— Young hyaline form : 2. hyaline form with beginning pigmentation ; 
3, pigmented form ; 4, full-grown pigmented form ; 5, 6, 7, 8, segmenting forms ; 9, 
extracellular pigmented form ; 10, flagellate form. 

Fig. 11.— Young hyaline form; 12, 13. pigmented forms; 14, fully-developed 
pigmented form ; 15, 16, segmenting forms : 17, flagellate form. 

"Figs. 18, 19, 20.— King-like and cross-like hyaline forms; 21, 22, pigmented 
forms; 23, 24, segmenting forms ; 25, 26, 27, crescents. 



18- is: 



to © 



23 24 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 283 



becomes motionless, and lines of radiate striation are formed in the 
organism, giving it a rosette-like figure composed of twelve to 
twenty parts. Segmentation proceeds until each of the segments 
becomes a small spherule. The corpuscle then bursts and the 
spherules or spores escape, probably to begin their cycle of develop- 
ment from the start by entering new red corpuscles as minute 
plasmodia. This cycle of development requires forty-eight hours. 

The Parasite of Quartan Malaria. — This is similar to the last 
named, but differs in the fact that the pigment-granules are much 
less abundant and coarser. The red corpuscle is not decolorized, 
as in the case of the tertian, but assumes a somewhat greenish 
hue. In about seventy-two hours segmentation occurs, six to ten 
segments and then spherules being formed. 

The Parasite of Irregular Malaria. — In the irregular malarial 
fevers of the summer and fall (the estivo-autumnal fevers) the 
organism is smaller than in the other cases, and rarely presents 
much pigment. The plasmodium frequently presents itself as a 
ring-shaped body, highly refractive and with a shaded central 
part. A few pigment-granules may be seen, but rarely more. 
The organism itself does not become larger than about one-third 
the diameter of the corpuscle in which it occurs. The red cor- 
puscle itself is greenish, as in the quartan variety. Segmentation 
is not observed in the circulating blood, though centrally placed 
pigment may be seen. The segmentation takes place in the spleen, 
bone-marrow, and other parts. The duration of the cycle of 
development is indefinite. 

Other Types Assumed by the Malarial Hematozoa. — Besides the 
regular forms described there is a flagellate variety, which is seen 
only in the blood kept for a little while outside the body. This is 
formed by the projection of thread-like processes which have 
active thrashing-movements. The pigment of the body itself is 
in the central part and is actively motile. These ciliated hema- 
tozoa may be found in tertian or quartan fever, but especially in 
irregular malaria. Recent observations on the blood of birds, as 
well as the studies of Manson and Ross in malaria, seem to show 
that the formation of these flagellated bodies is important in the 
reproduction of the organism. 

In the estivo-autumnal fevers a very curious form of the hema- 
tozoa is found ; this is the crescent form described by Laveran. It 
occurs in cases of some weeks' duration, and is developed within 
the corpuscles ; first, as a somewhat oval body, which becomes 
more and more crescentic, the pigment at the same time clumping 
in the center. The red corpuscle may entirely disappear, with the 
exception of a small portion seen in the concave part of the cres- 
cent as a mere shadoAv. 

The Organism Outside the Human Body. — It has been impossi- 
ble up to the present time to discover the malarial organism in 



284 



TEXT-BOOK OF PATHOLOGY. 



soil or water, and only a few uncertain observations of its occur- 
rence outside the body have been made. 

The Eelations of Mosquitoes to Malaria. — It has been shown 
experimentally that when certain mosquitoes are allowed to feed 
upon malarial patients and later upon healthy individuals, the 
latter acquire malaria in a certain proportion of cases. Some of 
the older experiments in this direction failed, and it has only 
recently been recognized that this was due to the fact that the 
mosquitoes employed in the experiments were of varieties that 
have no relation with malaria. The family of Anojjheles, and 
especially the Anopheles daviger, are the forms concerned. It has 
been found that the malarial organism in the stomach of the 
mosquito assumes the flagellate form, and certain pigmented 
bodies not occurring in the normal mosquito have been discovered 
in the walls of the stomach after the mosquito had fed upon 
malarial blood. Finally, the organism undergoes still further 
change, and is stored in the salivary glands of the mosquito, 
whence it is readily conveyed to the person subsequently stung. 
This extracorporeal cycle has been definitely proved, and there 
can be no doubt of this method of transmission. It explains 
very well certain well-known facts regarding the prevalence of 
malaria at certain seasons and at certain places. 

It is not certain, however, that malaria may not be trans- 
mitted in other ways. 

Pathologic Anatomy. — The most important fact in malarial 
infection is the destruction that it occasions in the blood. Rapid 
anemia with liberation of the hemoglobin (hemoglobinemia) and 
the appearance of granular pigment in the blood are among the 
results. The pigment accumulates in the spleen, liver, bone- 
marrow, and in other situations. Extreme disorganization of the 
blood may occasion hemoglobinuria and widespread pigmenta- 
tion. Congestive enlargement of the spleen, and, after long-con- 
tinued attacks, cirrhotic changes in that organ, may be observed. 
Thrombi of the capillaries and arterioles are not rare, and to 
these, in part at least, are due the focal necroses observed in the 
liver and elsewhere. 

Pathologic Physiology. — The curiously paroxysmal seiz- 
ures of malaria are probably the result of the liberation of toxic 
substances. The periodicity depends upon the duration of the 
cycle of development of the organism. A single group of tertian 
organisms cause a tertian fever (a paroxysm every other day). 
Infection with two groups of tertian organisms, maturing on alter- 
nate days, produces a quotidian fever (a paroxysm every day). 
One group of quartan organisms causes quartan fever (a paroxysm 
every third day) ; these groups (maturing on successive days) cause 
quotidian fever. 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 285 



Texas Fever of Cattle. — This disease is of interest in connection with 
malaria because of the relationship of the parasitic cause. The organism 
is a small, actively motile body which occupies the red blood-corpuscles. 
Frequently it occurs in pairs in the corpuscles, and the name Pyrosoma 
bigeminum was given to it on this account. Texas fever is characterized by 
acute fever and frequently by hemoglobinuria. The spleen is enlarged, and 
hemorrhages are observed in various organs of the body. When the blood 
of a diseased animal is injected into a healthy one, the latter acquires the 
disease. Transmission has been traced to the cattle tick {Ixodes bovis). 
When this is allowed to feed upon healthy animals after removal from dis- 
eased ones, transmission of the disease is observed. 

Sporozoa in Birds and Cold-blooded Animals. — Many blood parasites 
have been studied in birds, reptiles, and other cold-blooded animals. These 
are related to the sporozoa of malaria. 

COCCIDIUM OVIFORME. 

Description. — The coccidia are small bodies from 30 to 40 ft 
in length and from 15 to 20 ft in width, having a delicate outer 
coating, and within this a tough, double-contoured capsule. The 
body is filled with granular material, which is not rarely aggre- 
gated in the center. Outside the body sporulation takes place. 
The granular protoplasm divides into four rounded capsulated 
spores, each containing a granular resting body lying in the con- 
cavity between two sickle-shaped daughter-spores. Sometimes 
endogenous sporulation is said to occur, the parasite simply break- 
ing up into a large number of sickle-shaped bodies. The term 
jpsorospermice is applied to the rounded spores found in the coc- 
cidium (Fig. 112). 

Occurrence and Pathogenesis. — The coccidium is a fre- 




Fig. 112. — Coccidium ovifornie, showing method of reproduction. 



quent parasite of rabbits and certain other animals. It leads to 
the formation of yellowish nodules in the liver. It is an intra- 
cellular parasite, first invading the cells of the biliary passages 
and afterward the surrounding hepatic cells as well (Fig. 113). 
Less frequently it occurs in the intestinal tract, giving rise to 
nodular thickenings or ulcerations. 

The parasite escapes from the body in the stools and then un- 
dergoes sporulation. Other animals are probably infected by 
ingestion of the spores or sporulating coccidia. Occasionally the 
disease decimates rabbits or guinea-pigs kept in confinement. The 



286 



TEXT-BOOK OF PATHOLOGY. 



animals become languid, lose their appetite, emaciate, and have 
fever. Later they suffer from convulsions, stupor, or coma, and 
die in this condition. 

A few cases of coccidial disease of the liver have been observed 
in man. The lesions present themselves as cystic nodules spring- 
ing from the bile-ducts, or less commonly as a diffuse involvement 



vi 



'M 




V <s>\ " " *■ 

Fig. 113. — Coccidia in the wall of the bile-duct and the a 

rabbit. 



jacent hepatic structure of 



of the liver with cirrhosis and causing jaundice. Coccidial lesions 
of the intestines have also been discovered in man, and less com- 
monly invasion of the heart, of the kidneys, and other parts. 

The close association of the organism with the lesions, and the 
number of organisms discovered in the tissues, justify the belief 
that it is the specific cause of the lesions. 

The coccidium of the intestinal tract is generally smaller and 
the sporulation more rapid than that of the hepatic form. It was 
therefore supposed by Leuckart to be a special variety, and has 
been called Coccidium perforans. More recently this has been 
regarded as identical with the ordinary form. 

Eimeria Hominis. — Eimeria is characterized by the formation in each 
adult parasite of a single spore containing an indefinite number of 
sporozoites. The Eimeria hominis was discovered in the purulent exudate 
of a case of pleurisy. The spores were of large size and contained from ten 
to twenty sporozoites. accompanied by a protoplasmic remnant. The exact 
origin of the organisms in this case was not determined. Somewhat similar 
organisms were found by Virchow in a tumor of the liver, and by Severi in 
the lung. 

Sarcosporidia. — The sarcosporidia, also called Eainey's and Miescher's 
tubes, are met with in a number of mammals. The organism is composed 
of a protoplasmic mass covered with a capsule, and forming at the stage of 
maturity a large number of sickle-shaped or falciform sporozoites. The 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 287 



organisms usually occur in muscles, either within or between the muscle 
bundles, and are, therefore, elongated or tubular in shape. In connective 
tissues the organism may be rounded and sometimes grows to the size of a 
small cherry. Several varieties have been described, and a few observations 
have been made in man. 

ANIMAL PARASITES AND CARCINOMA. 

The theory that carcinoma and other malignant tumors are due 
to some form of infection is by no means of recent origin. Bac- 
teriologists sought to isolate micro-organisms without success ; and 
later observers have turned their attention to certain structures 
supposed to be animal organisms. 

In 1889 Thoma found in the protoplasm and nuclei of carci- 
noma-cells bodies which he regarded as coccidia ; and about the 




a b c d 

Fig. 114.— Inclusions in cancer-cells : a and 6, early stages of " parasitic " bodies ; c, 
late stages, showing division by segmentation ; d, cancer-cell containing leukocytes 
(Ruffer). 

same time Malassez and Albarran found similar structures in the 
cells of an epithelioma of the maxilla. Darier found bodies of 
the same kind in Paget' s disease of the nipple, and many sub- 
sequent investigators have described more or less similar forma- 
tions. 

Among these supposed protozoan organisms some are intranu- 
clear, some extra-nuclear, and some wholly extracellular. Among 
the intranuclear and extranuclear cell-inclosures Sjorbring de- 
scribed round bodies which tend to grow and eventually spor- 
ulate, forming cystic bodies containing twenty to thirty spores 
(spore-cysts). These structures resemble the parasites of silk- 
worm disease, and are classified by Sjorbring as microsporidia. 
Sudakewitsch and others have described bodies more closely 
resembling coccidia in their sharp, double contour and the pres- 
ence of peculiar, sometimes sickle-shaped, bodies within. Pod- 
wyssozki and Sawtschenko described forms differing from coccidia 
in the absence of a distinct capsule, and resembling rather the 
amebse, such as those occurring in the blood of birds and in 
malaria. The views of these authors, particularly Sawtschenko, 
have, however, undergone some modification in their several con- 
tributions. Ruffer, Plimmer, and Walker described structures 
occurring only in the protoplasm of the cells, and resembling 
coccidia, but forming neither spores nor sickle-shaped bodies, but 



288 



TEXT-BOOK OF PATHOLOGY. 



multiplying by direct division (Fig. 114). Many of the investi- 
gators lay stress upon the behavior of the supposed parasites 
toward stains. Thus Buffer and his collaborators point out that 
the nuclei of their parasites do not receive basic stains like cell- 
nuclei, but the acid-stains, and the body of the parasite is scarcely 
at all stained. This point, however, has certainly been overesti- 
mated as an indication of the parasitic nature of the bodies. De- 
generated cells notoriously vary from normal ones in this respect. 
The supposed spores of Sjorbring and others are very probably 
products of degeneration, as Buffer and others contend ; and it 
has not yet been shown by anyone that all of these supposed para- 
sites are not degenerated leukocytes or epithelial cells included 
within the cancer-cells or simple products of cell-degeneration. 

Some authorities have advanced a theory quite different from 
the above, holding that the cancer-cells themselves are parasitic 
organisms. Korotneff distinguishes three kinds of organisms in 
carcinoma : amebse, coccidia, and gregarinidse. The ameboid form, 
which he calls Amoeba cachexica, has a granular protoplasm and a 
clear nucleus. It is actively motile, and may leave the epithelial 
cells to enter the connective tissue. After establishing itself it 
becomes encysted, the nucleus breaking up and the protoplasm 
becoming more dense. Zooids and sporozooids result, the former 
going on to the formation of a gregarina(Rhopalo- 
cephalus carcinomatosus) (Fig. 115), or a coccid- 
ium, the latter forming new amebse. Some of 
the structures figured by Korotneff are undoubt- 
edly merely cancer-cells. A few authors claim 
to have found parasites of various kinds in the 
blood of cases of carcinoma. 

A close study of the so-called parasites of 
carcinoma shows that they are probably the re- 
sult of cell-degenerations. This is evident in 
part from the fact that they are most abundant 
in degenerated carcinomata or in degenerated 
areas of carcinomata, and from the very diver- 
gent character of the forms described. Further- 
more, similar structures occur in other tumors, 
some of them eminently benign, and even in 
ordinary inflammatory tissue. Russell, in 1890, 
described certain rounded bodies that stain intensely with fuchsin, 
and occur in or between the cells. These " fuchsin-bodies " are 
certainly not parasites, but cell-productions. 

Recently it has been urged that certain blastomycetes, resembling 
the ordinary yeast-fungus, if not identical with it, are the actual 
cause of cancer, and that many of the bodies formerly regarded as 
protozoa are blastomycetes. This view lacks confirmation. 




Fig. 115— Rhopa 
locephalus carcino 
matosus (Korotneff) 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 289 



ANIMAL PARASITES AND MOLLUSCUM CONTAGIOSUM. 

Definition. — Molluscum, or Epithelioma Contagiosum, is an 
infectious disease of the skin marked by the appearance of white 
and pink papules. 

Etiology. — The cause of this disease is, no doubt, a micro- 
organism of some sort. Its contagiousness is evidenced by the 
occurrence of epidemics in houses or asylums, by the occurrence 
of accidental inoculations, and by direct experiments. The incu- 
bation-period seems to be a long one — sometimes extending to 
several months. The lesions have been found to contain small 
bodies whose resemblance to coccidia was long ago pointed out 
by Virchow. It is uncertain whether these are really parasites or 
epithelial degenerations. Some authors are positive regarding the 
parasitic nature of the bodies ; others are equally convinced of 
their nonparasitic character. 

Appearances. — The disease occurs as single or, more fre- 
quently, multiple papules, at first quite small, but later becoming 
nodules of considerable size. In the larger a central depression or 
umbilication is seen, and on pressure cheesy matter may be ex- 
pressed from this. After reaching about 3 or 4 mm. in diameter 
they remain stationary, or undergo softening and suppuration. 
In exceptional cases the tumor may reach the size of a small 
orange. 

Seats. — The disease occurs on the face, neck, chest, genitals, 
or sometimes scattered over the whole body, sparing only the 
palms and soles. The lesions have occasionally been found on the 
mucous membranes. 

Structure. — Microscopically the lesions of this disease are 
found to consist of epithelial proliferations having a somewhat 
acinous arrangement, a hair-follicle occupying the center of each 
group of cells. The interior of the nodules is filled with soft, 
cheesy matter which may be expressed. The epithelial cells are 
arranged in several layers, the upper being normal cells with large 
nuclei, the deeper layers showing beside the nucleus small drop- 
lets, or rounded spherules, the so-called molluscum-bodies. These 
bodies grow in size, and may be so large as to fill the cell, pushing 
the protoplasm and nucleus to one side. In this process the cell- 
wall and protoplasm become horny, and practically the entire 
body consists of the enlarged molluscum-corpuscle. Certain 
granulations and more or less definite segmentations within these 
bodies have been described as sporulating conditions. The nature 
of these bodies is very doubtful ; they may be coccidia, gregarin- 
idse, or ameboid bodies ; but they may also, as some contend, be 
the results of epithelial degenerations. 

19 



290 



TEXT-BOOK OF PATHOLOGY. 



VARIOLA AND VACCINIA. 

A number of bacteria have been described from time to time 
in these diseases, and various micrococci in particular have been 
found in the pustules, but none of these can be considered as 
specific. Several bacilli, one form resembling the diphtheria 
bacillus, have been recently described. 

In 1887, Pfeiffer and van der Loeff independently described a 
protozoan parasite of the order sporozoa, which occurs in the cells 
of the rete. This organism was found in variola as well as in vac- 
cinia. Pfeiffer, Guarnieri, and other investigators found that by 
inoculation of the cornea of rabbits large numbers of the supposed 
parasites make their appearance in the epithelial cells. These organ- 
isms are rounded bodies lying in the protoplasm of the cells, some- 
times singly, sometimes in groups of two or three. Slow ameboid 
movements are visible and the organisms present one or more 
nuclei. Spore-formation has been observed by several investiga- 
tors. Guarnieri suggested the name ( 'ytoryctes variola? sen vaccina 1 . 
The nature and the significance of these supposed organisms have 
not yet been positively determined. Some authorities look upon 
them as products of cell-degeneration. 

Secondary infections with various micrococci or other organ- 
isms are common in small-pox and vaccination, and may play an 
important part in pustulation, and in the more definite complica- 
tions, such as septicemia, pneumonia, hemorrhagic septicemia, ery- 
sipelas, and the like. 

VARICELLA. 

The etiology of chicken-pox is even less definitely determined 
than that of small-pox. Pfeiffer discovered the same organism 
described by him in vaccinia and variola. Bacteria of one sort or 
another have been occasionally found. 

MEASLES, SCARLET FEVER, AND OTHER DISEASES. 

Certain investigators have discovered bodies having some of 
the appearances of protozoa in measles, scarlet fever, pernicious 
anemia, leukemia, sarcomata of various sorts, and in a number of 
other diseases. These observations, however, do not merit further 
discussion in this place. Future investigations must decide whether 
they have been accurate or not. 

CESTODES OR TAPE=WORMS. 

General Biology. — The life-history of the different forms 
of tape-worms is much the same. They have two states of exist- 
ence, the larval, which is generally found in one species of ani- 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 291 



mals (the intermediary host), and the adult state, usually occurring 
in another species (the host). It is supposed that in the case of 
one or two tape- worms an intermediary host is unnecessary, but 
this is doubtful. The adult worm, or tape-worm, occupies the 
intestinal tract of man or the lower (vertebrate) animals. It con- 
sists of a head, by which the worm fastens itself to the mucous 
surface ; and after the head, a neck of greater or less size and 
length, and a body consisting of separate links or proglottides. 
The latter represent complete organisms, containing a complicated 
genital apparatus, hermaphroditic in nature, which produces nu- 
merous eggs. The eggs are partly discharged from the segments in 
the intestinal tract through a genital pore, but especially escape 
into the outer world when the ripe segments are separated from 
the body of the worm, are discharged from the bowel, and subse- 
quently rupture and scatter the contained ova (Fig. 116). The egg 




1 2 3 

Fig. 116 —Segments of (1) Taenia saginata, (2) Bothriocephalus latus, and (3) Taenia solium, 
showing arrangement of uterus. 



or ovum encloses an immature larval organism, which, when 
received into a suitable intermediary host, penetrates the walls of 
the stomach or intestine and finds its way to the muscles or organs, 
where it imbeds itself and forms the well-known measles (see Figs. 
116 and 117). These are seen with the naked eye as small cyst- 
like bodies lying between the muscle-fibers. They contain a scolex 
or head, like that of the adult-worm, inverted into a sac filled with 
clear, watery liquid. When the measles or cysticerci occur in hol- 
low cavities, such as the ventricles of the brain, they may reach 
considerable size. They differ somewhat in different forms of 



292 



TEXT-BOOK OF PATHOLOGY. 



tape- worm, as will be described in connection, with the individual 
species. When flesh infested with larval tape-worms is eaten by 
man or some suitable animal, the cysts are dissolved and the scolex 
fastens itself upon the mucous membrane of the intestine. The 
body of the worm is then slowly or rapidly formed. 

Man is the host of tape-worms of adult or of larval type ; most 
frequently the former. In one case, the Taenia echinococcus, only 
the larval worm occurs in the human body, in the form of hydatid 
cysts. 

Pathologic Physiology. — Adult tape-worms may exist in the 
intestines of man without causing disturbances of any kind. Fre- 
quently, however, digestive disturbances and pain and various 
reflex manifestations arise. These may be caused by the action 
of the worm as a simple foreign body, or may result from 




Fig. 117.— Eggs of various worms found in the alimentary canal of man : a, Ascaris 
lumbricoides; b, C, Oxvuris vermicularis ; d, Triehocephalus dispar ; e, Anehvlostoma 
duodenale; f, Distoma hepaticum ; G, Distoma lanceolatum ; h, Taenia solium; i, Taenia 
saginata ; k, Bothriocephalus latus; X 400. 

poisonous agents generated by the worm in its normal life, or as a 
consequence of death and degeneration of the segments. When 
there are many worms (as in the case of Tcenia nana), the dis- 
turbances of digestion may be largely mechanical ; under similar 
circumstances, or when a single worm becomes coiled and forms a 
mass, intestinal obstruction may be occasioned. In the case of 
Bothriocephalus latus poisonous substances are undoubtedly pro- 
duced, and to these must be ascribed the severe forms of anemia 
caused by this worm. Other tape- worms rarely occasion anemia, 
and never the pernicious type just referred to. 

T/ENIA SOLIUM. 

This form occurs in the adult state in man as a worm two or 
three meters in length ; and in the hog or rarely in man in its 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 293 



larval condition. The bead is about the size of a pin-head and 
very dark. Anteriorly it has a rostellum armed with a double 
row of from twenty-six to thirty hook- 
lets. At the sides of the head are four 
suckers (Fig. 118). Attached to the 
head is a neck of thread-like appearance, 
w T hich terminates in the immature seg- 
ments of the anterior part of the body. 
The segments at first are broad and 
short, but become longer in proportion 
to the breadth toward the posterior end. 
The sexually mature segments are found 
at the middle and the posterior end of 
the worm. They contain a uterus consist- 
ing of a median tube and six to twelve 
lateral branches (Fig. 116). The genital 
pore is found at one side of the segment, fig. us —Head of Taenia solium 

f ill, , • • • (Mosler and Peiper). 

irregularly alternating m successive pro- 
glottides. The eggs, which may be squeezed from the segments 
or obtained free in the feces, are rather oval or spherical, from 30 
to 35 fi in diameter, and consist of a peripheral striated zone and 
a central granular portion, showing indistinctly six lines represent- 
ing booklets (Fig. 117). Groups of segments may be discharged 
from time to time, but this is not frequent ; the discharge of 
single segments is less frequent. The proglottides have indepen- 
dent movement, and may sometimes be seen to move about upon 
the bed-clothes. 

The I/arval State in Man. — When the ova are taken into 
the stomach the shell is digested and the embryo with its six 
hooklets is set free. This penetrates the wall of the stomach or 
intestine, and in some uncertain manner reaches the muscles or 
organs, where it eifects a lodgement. The hooklets are discarded 
and a little cyst containing clear liquid is formed, and at one point 
may be found a bud-like projection into the sac. This develops 
a scolex or head, which eventually becomes identical with the head 
of the fully formed worm. The cyst may be surrounded by a 
wall of reactive connective tissue. The duration of this process 
of formation of the cysticercus varies somewhat (five to ten or 
twelve weeks). The size of the cysts in the muscles varies from 
minute points to that of a pea. In the ventricles of the brain 
the cysticerci may be as large as a small cherry. Occasionally 
compound or racemose cysticerci are met with. 

Among the seats of special interest are the brain, the muscles, 
especially the peripheral muscles, tongue, and heart-muscle, and 
the subcutaneous tissues. 

The Adult Worm in Man. — When measled meat (hog, occa- 




294 



TEXT-BOOK OF PATHOLOGY. 



sionally that of deer, sheep, and other animals) is eaten in insuf- 
ficiently cooked form by man the capsules 
l#JiiilPiMll% UilPMW °f cysticerci (Fig. 119) are dissolved, 
1 l | j the scolex attaches itself to the mucous 
; , }||| membrane of the small intestine, and the 
L ' 7/ j | worm is developed. Usually there is but 
|1| If ;|l one worm ; occasionally several occur in the 

same case. The worm may remain in the 
j I ' ; ,jf/./ intestine for years, despite repeated efforts 
: ■ to dislodge it. In other cases it is spon- 
taneously discharged. Reverse peristalsis 
may cause portions to be carried to the 
stomach, whence they may be discharged 
by vomiting. In some cases the adult 
worm and the larval form have been 
found in the same individual (man). This 
is explained by the assumption that the 
eggs have reached the stomach, where the larvae have been set at 
liberty to penetrate the wall of the stomach and thus reach the 
tissues of the body. 

Geographical Distribution. — The Taenia solium is an ex- 
ceedingly rare parasite in America. It seems to be more common 
in certain parts of Europe. 



Fig. 119.— Measled pork ; two 
thirds the natural size (Leuck- 
art). 



TVENIA SAGINATA. 

This form is the common tape-worm of man. It is larger than 
the preceding form, being from four to eight meters in length. 
The head is large (2 mm. broad), cuboidal, and provided with 
four suckers. There is an abortive rostellum, but no hooklets 
(Fig. 120). The neck is short, and the segments rapidly become 




Fig. 120.— Head of Taenia saginata 
(Mosler and Peiper). 



Fig. 121.— Cysticercus Taenia? sagi- 
nata? ; natural size (Leuckart). 



broader than long, but in the posterior half of the worm, where 
the sexually mature proglottides are found, the segments are longer 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 295 



than broad. The uterus is formed like that of the Taenia solium, 
but the lateral branches are more numerous (twenty to thirty, and 
often dichotomously branched) (Fig. 116). The eggs are rather 
more oval and larger than those of Taenia solium, but otherwise 
closely resemble the latter. 

The larval form, or cysticercus, occurs in the ox and some- 
times in the giraffe. The measles are found in the muscles, liver, 
lungs, and occasionally in other organs (Fig. 121). 

The adult form occurs only in man, and occupies the small 
intestine. The presence of the worm does not seem to occasion 
any definite disease of the intestines, except in rare cases, when a 
number are found present in a coiled mass, or when one worm is 
similarly coiled. This may cause intestinal obstruction, and pos- 
sibly in exceptional instances rupture of the bowel. 

The symptoms ascribed to tape-worms are some of them doubt- 
less reflex ; but it is noteworthy that they are often absent until 
the patient discovers segments in the stools. (Further refer- 
ence to possible pathologic results is made in the discussion of 
Bothriocephalus latus.) It is an exceedingly 
common parasite in certain countries (Africa 
and the East), but is more or less commonly 
found in all parts of the world. 



TAENIA NANA. 

This form, sometimes called the dwarf 
tape-worm, in its adult state is about 2.5 cm. 
in length (Figs. 122 and 123). It has a 
rounded head, with a rostellum that may be 
protruded or retracted and that bears a single 
circle of twenty-two to twenty-seven hook- 
lets. The mature segments of the posterior 
end of the worm have a yellow color. The 
genital pore is on the 
same side in all the seg- 
ments. The eggs are o val 
in shape, whitish and 
transparent ; they are 
from 47 to 48 fi long 
and 38 to 39 a broad. 

The intermediary host 
of this form is not cer- 
tainly known, but is sup- 
posed to be some form 
of insect or snail. In the 
rat the larval form occurs in the intestinal w r alls 
at the base of the villi in the form of a cysti- 




Fig. 122.— Taenia nana 
about natural size (Mos 
ler and Peiper). 



Fig. 123 —Taenia nana, 
much enlarged (Mosler 
and Peiper). 



296 



TEXT-BOOK OF PATHOLOGY. 



ceroid, which later discharges its contained embryo into the intes- 
tine, where it matures. The same sequence may occur in man. The 
adult parasite alone occurs in man. The head attaches itself deeply 
in the mucous membrane of the bowel, and may cause considerable 
local disturbance. There are usually several or many worms asso- 
ciated ; sometimes there may be several thousands. 



Fig. 124.-' 
(Mosler 



fsenia elliptica 
and Peiper). 



T7ENIA ELLIPTICA. 

This form is identical with Tcenia cueu- 
merina. It is a common parasite of dogs 
and cats. The length is from 15 to 30 cm. ; 
the head is provided with a rostellum bear- 
ing sixty booklets ranged in four rows ; the 
rostellum may be protruded or retracted. At 
the junction of the segments there is a consid- 
erable contraction of the diameter of the worm, 
giving the body a markedly linked character 
(Fig. 1 24). The mature segments have a red- 
dish-brown color from the presence of the eggs. 
Each proglottide has a double sexual appa- 
ratus with a genital pore at each side. The 
intermediary host is probably the louse of 
the dog and occasionally the flea. The adult 
worm usually occurs in numbers in the intes- 
tinal tract, and in some cases seems to pro- 
duce inflammatory disturbances. 



TVENIA FLAVOPUNCTATA. 

This form (probably identical with Taenia diminuta) is from 
20 to 30 cm. in length ; the head is elongated and verges gradu- 
ally into the neck. The suckers are small, but there is neither 
rostellum nor hooklets. The segments are marked by a yellowish 
spot which represents the male genital organs. 



TVENIA MADAGASCARIENSIS. 

This form is from 25 to 30 cm. in length ; the head is marked 
by four large suckers and a rostellum bearing hooklets. 



OTHER FORMS OF T/ENIA. 

Besides these more or less satisfactorily described forms, a 
number of uncertain varieties have been reported, such as the 
Tcenia tenella, Tcenia Algeriana, etc. 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 297 



T/ENIA ECHINOCOCCUS. 

The Tamia echinococcus in its adult form occurs in the intes- 
tinal tract of the dog, the larval condition occurring in man and in 
some of the lower animals. The mature worm is, about 4 or 5 
mm. in length, and consists of four segments (Fig. 125). The 
head, which constitutes the first, is provided with four suckers and 
a rostellum bearing fourteen to twenty-five booklets in a double 
row. The second segment is about the breadth of the head, but 
somewhat shorter. The third is considerably larger ; and the 
fourth is the largest of all, constituting about 
one-half or two-thirds of the entire worm. The 
uterus consists of a median portion Avith few 
lateral branches. The eggs are oval, from 17 
to 30 /j. in diameter, and the shell is rather 
thinner than in the eggs of other tape-worms. 

The adult worm occurs in great numbers in 
the small intestine of the dog. It is also found 
in the wolf and fox, and occasionally in other 
animals. 

The Bchinococcus Cyst. — This term is 
applied to the structure in which the larval 
worm is embedded. Three varieties have been 
distinguished. 

(a) Echinococcus Scolicipariens. — When the 
eggs reach the stomach of man the embryo is 
freed and penetrates the mucous membrane. It is carried by the 
blood or lymphatic stream to the liver or other organs, where it 
develops an eckinococcus-cyst (Fig. 126). 




Fig. 125.— Taenia echi- 
nococcus ; enlarged 
(Hosier and Peiper). 




Fig. 126. — Echinococcus-cyst of the liver (from a specimen in the Museum of the Phila- 
delphia Hospital.) 

The wall of the cyst is composed of two layers, an outer cuticular 
and an inner parenchymatous, granulocellular layer. The paren- 



298 



TEXT-BOOK OF PATHOLOGY. 



chymatous layer is important as a budding or brood-membrane. 
After some weeks there may be seen upon its surface small buds 
or projections, which later become hollowed by a central excava- 
tion and form a small cyst ; secondary budlets spring from the 
surface of this and gradually form embryonal heads or scolices 
(Fig. 127). When mature these are retracted or inverted into 
the cavity or cyst of the original bud. In this manner a large 
number of heads are formed upon the inner wall of the original 
echinococcus-cyst, the cavity of the cyst at the same time increas- 
ing in size and being distended with characteristic liquid. This 
is a clear fluid, having a specific gravity of 
from 1009 to 1015 and a neutral or alka- 
line reaction, and containing no albumin or 
only traces, but a considerable quantity of 
chlorid of sodium. Sugar is sometimes 
found in the fluid. 

{b) Echinococcus Hydatidosus. — Besides 
fig. 127 -Formation of this form of simple cyst with buds attached 

buds upon the parenchyma- . vi 1 • i • i 

tous layer (Leuckart). " to the inner wall, there are cases m which 
daughter-cysts and even granddaughter- 
cysts are formed. The daughter-cysts are found within the original 
cyst, and are probably produced by cystic degeneration of the buds 
already described ; and possibly in some cases by simple separation 
of the buds. They are variable in size, sometimes becoming as 
large as a nut or egg, and when granddaughter-cysts are contained 
within them the size may be even greater. To this form the term 
Echinococcus hydatidosus or Echinococcus endogenes is applicable. 

In a subvariety of this form secondary cysts are produced out- 
side the original wall. These are formed by a process of soft- 
ening in the cuticular wall, with gradual projection of the paren- 
chymatous layer toward the exterior and eventual rupture, with 
formation of secondary cysts outside. 

(c) Echinococcus Multilocularis. — In a third form of echinococ- 
cus-disease there are numerous small cysts, from the size of a 
grape-seed to that of a pea, embedded in connective tissue, and 
altogether forming a more or less definite tumor-mass. On sec- 
tion this presents an alveolar appearance, the cysts containing 
somewhat gelatinous material. Careful examination of the inner 
walls of the small cysts shows them to contain pigment and cal- 
careous particles. Scolices, however, are absent for the most part, 
the cysts being generally sterile. The term Echinococcus mirfti- 
locularis is applied to this variety of disease (Fig. 128), Its forma- 
tion is explained by the assumption that there are secondary pro- 
liferations in an outward direction from the original cyst, rather 
than a deposit of large numbers of ova or embryos. The whole 
mass presents the appearance of a tumor, and not rarely central 
necrosis and softening occur as in tumors. 




ANIMAL PARASITES AXD DISEASES CAUSED BY THEM. 299 



Echinococcus cysts may continue to grow until they have reached 
huge dimensions without undergoing any secondary changes. In 
other cases the parasite may die and the growth may cease, 
or active proliferation of the tissues around the cyst may lead to 
early destruction. In still other cases suppurative change occurs 
in the cyst or its wall. In all cases when the cyst reaches a cer- 
tain size the tissues around produce a connective-tissue capsule of 
greater or less thickness. When the parasite dies inspissation of 
the liquid occurs, and it may eventually disappear or be converted 
into a thick whitish material; the cyst-walls and the connective- 




Pig. 128.— Echinococcus multiloeularis (Luschka). 

tissue capsule at the same time shrivel and present peculiar con- 
centric lamellations that are very characteristic. Eventually cal- 
cification of the wall of the cyst and to a certain extent of its 
contents takes place. 

Seats. — Echinococcus cysts are most frequent in the liver. 
They also occur in the lungs, kidneys, spleen, and omentum, and 
less frequently in the brain or other parts of the nervous system. 
The pathologic effects are produced by direct mechanical pressure. 

The geographical distribution is extensive, but the dis- 
ease is common only in restricted localities, especially in northern 
countries (north of Europe, Iceland). 

BOTHRIOCEPHALUS LATUS. 

The Bothriocephalic latus is the largest tape- worm of man, 
reaching the length of from 5 to 9 m. The head is flattened 
and club-shaped and presents two groove-like suckers at its sides 
(Fig. 129). The neck is thin and gradually increases in diameter. 
The ripe segments are quadrate, and are distinguished by a rosette- 
like formation of the uterus, which is plainly visible in the center 
of each proglottid (Fig. 116). The genital pore is upon the flat 
surface of the segment and always upon the same side of the 
worm. The eggs are oval in shape and enclosed in a shell pre- 
senting a hinged lid at one pole. The intermediary host is some 
form of fish, most frequently the pike. The eggs first undergo a 



300 



TEXT-BOOK OF PATHOLOGY. 



certain amount of development in water, the embryo becoming 
free and floating about or being propelled by a ciliated outer 
covering and then entering the digestive tract 
of fish. 

The geographical distribution is com- 
paratively restricted. It is frequent in certain 
northern countries, as in Sweden, and in parts 
of central Europe, especially in Switzerland. 
It is only occasionally met Avith in America in 
immigrants. 




Fig. 129.— Head and 
neck of Bothriocepha- 
lus latus (Leuckart). 



BOTHRIOCEPHALUS CORDATUS. 



This variety is much smaller than the last, 
the maximum being from 1 to 1.25 p.. The 
head is short, broad, and heart-shaped, and the suckers are placed 
upon the flat surface. The uterine structure differs from that of 
Bothriocephalic latus in being narrower and more elongated, and 
also in having lateral branches. The body of the worm contains 
granular calcareous matter. 



BOTHRIOCEPHALUS CRIST ATUS. 

This form is about 3 m. in length, and is distinguished by two 
crest-like projections upon the head. These are covered with 
numerous small papillae. There are no definite suckers, and the 
head contains abundant granular calcareous matter. 



BOTHRIOCEPHALUS LIGULOIDES. 

This variety occurs only in the larval form in man. It has 
been found in the region of the loins and in the tissues about the 
eyes. The head of the worm is distinguished by a papilla-like 
projection. 

NEMATODES, OR ROUND=WORMS. 



ASCARIS LUMBRICOIDES. 

The Ascaris lumbricoides, or ordinary round-worm, is one of 
the most frequent intestinal parasites. The male may reach a 
length of 25 cm. and a thickness of 2 to 4 mm. ; the female is 
longer, up to 40 cm., and thicker, up to 5 or 6 mm. The body 
of the worm is brownish or sometimes pinkish in color, and pre- 
sents parallel ridges or rings somewhat like those of the earth- 
worm. The head is provided with three rounded prominences or 
lips, between which the mouth is placed (Fig. 130). The male 
shows two chitinous spicules at the cloaca. The eggs of the worm 
are produced in great numbers ; they are covered with a tough 
shell, and surrounding this is a clear material in an irregular mass. 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 301 







The contents of the eggs consist of a granular material, sometimes 
showing the linear outlines of an embryo. 

The ascaris develops in man from swallowing of the eggs in 
infested drinking-water or food. The parasites may be present 
singly or in numbers. They occupy the 
small intestine, but frequently migrate, 
entering the gall-ducts, the stomach, the 
esophagus, and even the larynx or nasal 
cavities. 

Pathologic Physiology. — Ascarides 
may give rise to violent symptoms by ob- 
struction of various passage-ways, and when 
in numbers or united in masses even intes- 
tinal obstruction may be caused. It is 
probable that ascarides produce irritating 
secretions, as it has been observed that 
considerable dermatitis sometimes arises 
in persons handling them. Occasionally 
abscess-cavities containing lumbricoids are 
found in connection with ulcerations and 
perforation of the intestines. These ab- 
scesses were believed by older authors to be 
caused by the worms ; at the present time 
it is more generally held that the worms 
play no important part, their presence 
being due only to their coincidence in the 
intestine. 

ASCARIS MYSTAX. 

This form, which is common in cats 
and do£S, is rarelv met with in man. It 
is much smaller than the ordinary round- 
worm, the male reaching a length of 45 
or 60 mm., and the female 120 or 130 
mm. The head is distinguished by two 
lateral wing-like projections composed 




Fig. 

coides : 



130.— Ascaris lumbri- 
A, female : B. male ; C. 
rnified 300 diameters; 



b, head, magnified (after Perls). 

of chitinous material. 



ASCARIS MARATIMA. 

This form has been observed but once, and the female alone 
was found. 



OXYURIS VERMICULARIS. 

The oxyuris, seat-worm, or pin-worm, is one of the commonest 
parasites of man. The male is 2.5 to 5 mm. in length ; the female, 
10 to 12 mm. (Fig. 131). The posterior end of the male is blunt 
and curved upon itself; in the female it is elongated. The eggs 
of the oxyuris, which are produced in great numbers, are oval or 



302 



TEXT-BOOK OF PATHOLOGY. 



elliptical and about 5 fx long. The embryo is visible within as 
a lobulated body. The parasite is developed directly from the 
eggs. When these are swallowed the outer coating is dissolved 
in the stomach and the embryos escape, to reach their full de- 
velopment in the small intestine. The impregnation occurs in 
the small intestine and within a short time after the swallowing 
of the eggs. After impregnation and ripening the female para- 
sites move toward the rectum and may be discharged, or may 
leave by their own movements. The life 
of the worm is short, but there is always 
the possibility of reinfection. 

Oxyuris is especially common in child- 
hood. It is probable that the worms 
sometimes cause inflammatory troubles. 
In cases in which they accumulate innum- 
fig. i3i.-oxyuris vermicu- bers a form of verminous diarrhea may be 

laris: a, female ; 6, male (Mos- , -. T n , , , ■ ... 

ler and Peiper). produced. In female children vaginitis 

frequently results from the migration 
of the parasites into the vagina. 

TRICHINA SPIRALIS. 

The Trichina spiralis occurs in its larval form in the muscles 
or organs of man and in the lower animals ; in the adult form it is 
found in the intestines of man or animals. 

The adult male is about 1.5 mm. in length and 0.14 mm. in 
thickness. At the posterior end there is a retractile cloaca flanked 
by two projections. The female is 2 to 4 mm. in length and 0.6 
mm. in thickness. The eggs are provided with a very thin shell, 
and the embryos escape from this within the uterus. They are 
produced in immense numbers. The young embryos found in the 
intestinal tract are from 0.1 to 0.16 mm. in length, the anterior 
end thicker than the posterior. In part they escape with the 

feces, and die ; the greater part pene- 
trate the intestinal wall and are car- 
ried to various parts of the system, 
embedding themselves especially in 
the muscles, where they undergo 
further changes. Here the organism 
coils itself and becomes surrounded 
with a capsule, which is at first trans- 
parent, but may subsequently undergo 
calcareous change and become opaque 
(Fig. 132). 

Trichina? are acquired by man by 
eating improperly cooked ham. The 
capsules are digested and the larval trichinae set free. In the 




a b 




Fig. 132. — Trichina-capsule with 
its connective-tissue covering : a, 
early stage ; b, calcined (Leuckart). 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 303 



small intestine they reach their maturity in about three days ; the 
females are impregnated, and some days later discharge the em- 
bryos, some of which die or escape with the feces, while others 
probably bore their way into the mucous membrane. Many of 
the females penetrate the intestinal walls, and especially the 
lymphatic tissues of the walls, where thty liberate their embryos. 
These are disseminated throughout the body by their own migra- 
tions or with the lymph- and blood-streams. 

The favorite seat is the striated muscle-tissue, and they lie 
within the muscle-bundles themselves or less frequently between 
them. They reach their destination in ten days after the primary 
invasion, but subsequent crops are deposited as the young continue 
to mature in the intestines. In two or three weeks they begin to 
become encysted in the muscles. 

When the embryos are liberated in the stomach and intestines 
they occasion violent gastro-intestinal irritation, with vomiting, 
diarrhea, and often more or less pronounced collapse. In their 
later migration the worms set up intense muscular pains of rheu- 
matoid character, with edematous swelling and fever. 

Trichiniasis is common in all parts of the world, but has been 
largely reduced by greater care in the cooking of pork. 

ANKYLOSTOMA DUODENALE. 

The Ankylostoma duodenale, or Dochmius duodenalis, is a 
cylindrical worm, the female being from 7 to 16.5 mm. in length ; 
the male, from 7 to 11.2 mm. The head is rounded, and is armed 




Fig. 133.— Anchylostoma duodenale: a, male, natural size : b, female, natural size ; c.male 
magnified; d, female magnified; e, head, greatly magnified ; /, eggs (von Jakseh). 

with six sharp, hook-like teeth. The female is usually of a brown- 
ish or reddish color, due to absorption of coloring-matter of the 
blood. The eggs are easily distinguished, being elliptical-shaped, 



304 



TEXT-BOOK OF PATHOLOGY. 



from 0.056 to 0.063 mm. in length and 0.036 to 0.04 mm. in 
thickness. The shell is separated from the contents, and the latter 
have a granular appearance, are brownish, and in the state of 
segmentation. The eggs may appear in the stools in great num- 
bers. The embryo is fully developed outside the body, and entering 
the stomach and intestines of man there undergoes full develop- 
ment (Fig. 133). 

The adult worm occupies the small intestine. It may be 
present in small or large numbers, and is usually rather firmly 
attached to the mucous membrane. Changes in the latter, how- 
ever, are not pronounced. 

Patients harboring this parasite frequently become intensely 
anemic. It was this parasite which was found in many cases of 
Egyptian chlorosis, and it is the same organism that produced the 
intense anemias (pernicious anemia) of the laborers engaged in 
building the St. Gotthard tunnel. 

ANGUILLULA INTESTINALIS AND STERCORALS. 

The Anguillula intestinalis occupies the intestinal tract and the 
ducts communicating with it. It is an actively motile, cylindrical 
organism about 2 mm. in length. Only a female form exists ; 
this by parthenogenesis producing eggs from which male and 
female embryos are developed. The latter in their adult form 
differ from the original worm and were regarded as a different 
organism — Anguillula stercoralis. These are never found in fresh 
feces, and in autopsies only when this has been delayed some time 
after death. The male is somewhat smaller than the female. In 
the latter the posterior extremity is drawn out to a fine point and 
straight ; in the former it is thicker and curled upon itself. Be- 
sides this distinction the male bears two spicules projecting from 
the cloaca. The embryos formed by the Anguillula stercoralis de- 
velop into the original form, the female Anguillula stercoralis. 
Besides this method of indirect reproduction through the stage 
of A. stercoralis, direct formation of A. intestinalis may occur. 

These organisms have been found with special frequency in 
Cochin China and other eastern countries, occurring in the 
intestinal tract in cases of severe diarrhea. It is doubtful whether 
they have definite pathologic significance. 

TRICHOCEPHALUS DISPAR. 

The anterior portion of this parasite is thin and thread-like, 
while the posterior portion is thicker. The length of the worm is 
from 4 to 5 cm., the male being somewhat the smaller. The 
thicker part of the male is curled upon itself and blunt at the 
end, while that of the female is straight and more pointed. The 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 305 



eggs are very characteristic, being brownish in color, covered with 
a thick capsule, and having at either pole a button-like projection 
(Fig. 117). The length of the egg is about 0.55 mm. 

The parasite occupies the cecum in man, occasionally the vermi- 
form appendix, and sometimes the small intestine. It is particu- 
larly frequent in children in Syria and Egypt. It does not, as a 




Fig. 134.— Trichocephalus clispar ; natural size (Heller). 

rule, produce serious disturbance, but may cause intestinal or 
reflex nervous symptoms. Recently it has been claimed that the 
parasite causes considerable disturbance by abstracting blood. 



FILARIA MEDINENSIS. 

The Filaria or Dracunculus Medinensis is a round-worm in- 
festing the subcutaneous tissues and the skin. The male has not 
been recognized with certainty, though two recent observers have 
found a smaller, degenerated and partly calcified form in associa- 
tion with the female filaria. The female sometimes reaches a 
length of 60 to 80 cm.; it is yellowish in color and exceedingly 
elastic. In general appearance it resembles a string of catgut. 
The body of the worm contains a highly developed uterus, 
which practically fills the cavity of the worm, the intestinal 
tube being crowded to one side. The uterus is found to contain 
innumerable small embryos ; these escape when the parasite is 
ruptured. 

The organism occurs very abundantly in tropical countries of 
the old world, notably Arabia, along the coast of the Caspian Sea, 
in Abyssinia, and Guinea. The parasite is sometimes called the 
Guinea- worm. 

The parasite infests the subcutaneous. tissues, particularly those 
of the lower extremities, and gives rise to inflammatory lesions 
resembling carbuncles. The method of invasion and the life-his- 
tory of the organism are obscure. It has been held that the 
embryos develop in water of swamps, and enter directly through 
the skin. This view has never been proved, and recent investi- 
gations would indicate that certain crustaceans of the family 
Cyclops are the intermediary host and effect the transmission to 
man. Some authorities believe that the invasion occurs through 
the gastro-intestinal tract. 

20 



306 



TEXT-BOOK OF PATHOLOGY. 



FILARIA SANGUINIS HOMINIS. 

Several varieties of filarial have been found in the blood and 
are included under this generic term. The discovery of the 
organism, or rather of the embryos, was made by Wueherer, in a 
case of hematuria. 

The embryos appear in the blood, urine, the lymph, and the 
tissues as thread-like structures, varying in size in the different 
varieties. The ordinary form has a thickness of about the 
diameter of a red corpuscle, and is as much as 0.2 to 0.5 mm. 
in length. It consists of a transparent sheath, almost completely 
filled with the embryo, the ends, however, projecting a little 
beyond the organism, in a sac-like fashion (Fig. 135). The em- 
bryo is actively motile, squirming, thrashing, or curling and un- 
curling itself rapidly, and thus producing more or less agitation 
of the corpuscles or solid bodies in its vicinity. 

The number of the embryos found in the blood varies greatly ; 
in many cases a search through several cover-glass preparations 
may be necessary to detect a single one. Usually they are more 




Fig. 135.— Filaria embryo, alive in the blood (F. P. Henry). 



abundant. A feature of importance is that they occur only during 
the night, unless the patient reverses the usual conditions and rests 
during the day. 

The adult worms occupy the lymphatic channels, the male and 
female being found together. The male is somewhat smaller than 
the female and is colorless. The brownish-colored female worm 
is about 38 mm. in length and produces embryos in great abun- 
dance. These enter the circulation and are discharged in various 
w T ays, especially in the urine. The mosquito has been found to act 
as the intermediary host in which the embryo reaches its fuller 
development. 

Filariasis is particularly common in the warmer climates, but 
is occasionally met with in this country, especially in the Southern 
States. One' of its most frequent forms is characterized clinically 
by hematochyluria. The embryos in these cases may be found in 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 307 



the blood and also in the chylous urine. Pathologically no gross 
changes may be found, but there may be in other cases evident 
distention of the lymphatic channels and blood-vessels of the 
pelvis of the kidneys, ureters, or bladder ; and the embryos may 
be found in the substance of the kidneys or in the walls of the 
blood-vessels. Another form of filariasis is elephantiasis. In 
these cases there is obstruction of the lymphatic vessels in con- 
sequence of the presence of the parasites, of thrombi, or of inflam- 
matory lesions, and as a result of these conditions dilatation of the 
peripheral lymphatic vessels occurs. The skin may be ruptured 
and chylous liquid may exude. The embryos may be found in 
this on microscopic examination. 

Varieties. — Manson has described three varieties of embryonal 
filaria3 — 'the original form, or Filaria noeturna; a second variety, 
in which the embryos are found at any time, night or day, called 
Filaria perstans, which he believes the cause of the sleeping- 
disease of Africa as well as of certain skin diseases (Craw-Craw) ; 
the adult worm is unknown. The third form is the Filaria 
diurna, which appears in the blood only during the day. The 
last is probably the embryo of Filaria loa, a form occurring in 
the eye, lying under the conjunctiva. It is found in Africa and 
tropical America. Manson believes that the mangrove fly is the 
intermediary host. 

OTHER FORMS OF FILARL4E. 

The Filaria lentis was found in the lens in a case of cataract. 
The Filaria labialis was discovered in a pustule on the lip of a 
student in Naples ; the Filaria hominis oris was found by Leidy 
in the mouth of a child ; and Filaria restiformis was found in the 
urine of a patient by the same observer. The Filaria immitis 
is the common filaria of the dog, and has been found in man. 
The Filaria bronchialis was found in bronchial lymphatic glands 
in a case of phthisis, and has also been found in the trachea and 
bronchi. The Filaria Demarquayi and F. Magalhwsi are forms 
whose identity has not been sufficiently established. Filaria con- 
junctivae, F. lymphatica, and F. Romanorum-orientalis are others 
that have been described. 

ECHINORRHYNCHUS GIGAS. 

This is a large round- worm, the body being marked by distinct, 
transverse, parallel rings. The male may be from 7 to 10 cm. in 
length, the female from 31 to 50 cm. There is a retractile rostel- 
lum, with six rows of hooklets, at the anterior end, each row com- 
posed of eight spicules. The parasite occupies the small intestine 
of the hog, and has been found occasionally in man. The inter- 
mediate host seems to be the grub of the cockchafer and the J une- 
bug. 



308 



TEXT-BOOK OF PATHOLOGY. 



Other varieties of echinorrhynchus have been described, but 
are not well-determined species. 

EUSTRONGYLUS GIGAS. 

The female of this species may reach a length of 1 m. ; the 
male is but one-third this size. The anterior end of the worm 
is retracted, and the mouth surrounded by six papillae. The 
posterior end is expanded, and provided with a ^spicule projecting 
from the cloaca. The color of the worm is brownish or blood-red. 
The parasite is found in the pelvis of the kidneys, ureters, and 
bladder of dogs, horses, cattle, and other animals, and rarely in 
man. Among its results are enlargement of the pelvis of the 
kidney and atrophy of the kidney-substance. 



STRONGYLUS LONGEVAGINATUS. 

This parasite was found in the lungs of a child. It resembles 
the strongylus met with in the lungs of sheep and other animals. 



TREMATODES, OR FLUKE=WORMS. 

The fluke-worms are usually flattened organisms, somewhat 
tongue-shaped and provided with powerful suckers and occasion- 
ally also with hooklets. The intestinal canal begins in the oral 
orifice anteriorly, but is closed at the posterior extremity. Repro- 
duction may take place directly or by the formation of an inter- 
mediate organism which is parasitic to certain lower animals. In 
this stage they are actively motile, swimming about in water, and 
are known as the cercarise. 



D I STOMA HEPATICUM. 



The Distoma hepaticum, or liver-fluke, is from 15 to 35 mm. in 
length and 6 to 20 mm. broad ; it is pointed at either end, and an- 
teriorly is provided with two suckers, one 
at the head and one upon the ventral sur- 
face, somewhat posterior to the first (Fig. 
136). The genital pore lies between the 
two suckers. The eggs are oval in shape, 
0.14 to 0.15 mm. in length, and provided 
with a lid at one pole. 

The adult organism occupies the biliary 
ducts and is a frequent parasite of sheep. 
It is occasionally met with in man, usually 
occurring in considerable numbers. It 
gives rise to obstruction of the biliary 
passages and consequent enlargement, con- 
gestion, and later degeneration of the liver. The gall-ducts above 



mm 



Fig. 136— Distoma hepati- 
cum; two-thirds the natural 
bize (Mosler and Peiperj. 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM 309 



the point of obstruction have sometimes been found considerably 
dilated or cystic. Clinically ascites and jaundice have been found, 
with gastro- intestinal symptoms and distoma-eggs in the stools. 



DISTOMA LANCEOLATUM. 

This form is smaller than the last, 8 to 10 mm. in length and 
2 to 2.5 mm. in breadth. The two suckers are far apart, and the 
genital pore lies between them (Fig. 137). 
The eggs are 0.04 to 0.05 mm. in length 
and 0.03 mm. in breadth. 

This form is frequently associated with 
the last, and occupies the biliary passages of 
sheep and cattle. It is occasionally met 
with in other animals and in man. 




DISTOMA HEMATOBIUM. 



Fig. 137 —Distoma lan- 
ceolatum ; two-thirds the 
natural size (Mosler and 
Peiper). 



This organism occurs in sexually distinct 
forms ; the male and female, however, oc- 
curring together. The male is 12 to 14 mm. in length and 1 mm. 
thick, and the posterior part is somewhat flattened and curved 
ventralward to form a groove, in which the female is attached 
(Fig. 138). The latter is 16 to 18 mm. long, and 0.13 mm. thick. 
The eggs are 0.12 mm. long and 0.04 mm. broad, and drawn out 




Fig. 138.— Distoma hematobium, with eggs (von Jalrsch). 



to a point at one end. The adult parasite occupies the portal vein 
and the veins of the spleen, mesentery, and the plexuses of the 
bladder and rectum. The eggs of the organism may be found in 
any of the organs, notably in the liver, in the intestinal walls, and 
in the mucous membranes of the urinary passages. They prob- 
ably occupy the vascular system ordinarily, but cause rupture of 
the walls of the vessels and thus escape into the tissues. 

The pathologic changes caused by this parasite are most strik- 
ingly seen in the ureters and bladder in acute cases. Hyperemic 
spots or small hemorrhages may be seen in the mucous membrane, 
and the surface is covered with blood-stained mucus containing 
the eggs. In cases of longer standing roughness of the mucous 
membranes and usually small ecchymotic elevations or outgrowths, 



310 



TEXT-BOOK OF PATHOLOGY. 



suggesting papillomata, are observed (Fig. 139). Section through 
these shows that they consist of proliferated cells with enlarged 

blood-vessels, from which the adult worm 
may be removed. The tissues surround- 
ing the vessels may contain eggs in enor- 
mous numbers. The mucous membrane 
is frequently covered with a calcareous 
deposit composed of urate and oxalate 
of sodium, and the excrescences may be 
converted into calcified polyps. Among 
the final results may be cicatricial strict- 
ures of the ureter, pyelitis, and distention 
of the pelvis of the kidney, with atrophy 
of the kidney-substance. Similar patho- 
logic processes may be found in the rec- 
tum. When the portal vein is occupied 
the eggs of the distoma may be abundant 
in the liver-substance. Distoma hema- 
tobium is a parasite occurring with enor- 
mous frequency in Northern Africa and 
neighboring countries. It is compara- 
tively rare in other parts of the world. 




Fig. 139.— Papillary thicken- 
ing of the mucous membrane 
of the bladder, showing dis- 
toma-eggs in site (Mosler and 
Peiper). 



DISTOMA PULMONALE. 

This organism is from 8 to 10 mm. in 
length and from 5 to 6 mm. in breadth. The eggs are brownish, 
and from 0.08 to 0.1 mm. in length. The worm occurs in the 
lungs, occupying excavated spaces, usually near the periphery of 
the organ. These cavities contain reddish or quite hemorrhagic 
mucopurulent liquid and abundant eggs. The cavities are in com- 
munication with the bronchi, and clinically the disease is marked 
by cough and hemorrhagic expectoration or even repeated hemopty- 
sis. This parasite occurs very frequently in Japan, China, and Corea. 

OTHER FLUKE=WORMS. 

Among other forms of distoma of less importance are Distoma 
crassum, met with a few times in the intestine ; Distoma hetero- 
phyes; Distoma ophthalmobium, found in the lens of the eye ; Dis- 
toma sinese, found in the liver ; Distoma eonjunetum, also occurring 
in the liver ; and the Moiiostoma Jmtis, occurring in the eye. The 
Amphistoma hominis occurs in the intestinal tract. Two forms, 
the Hexathyridium venarum and Hexathyridium pinguicola, are 
possibly forms of encapsulated Distoma hepaticum. 

ANNELIDES. 

Two forms of leeches are of some pathologic importance. The 
Hirudo Ceylonica is a form occurring with great frequency in 
Ceylon and other islands and in parts of South America. It is 



ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 311 



found in vegetation, and attaches itself to the skin of the legs and 
to other parts of man by means of a sucker and its short teeth. 
It may give rise to painful ulcerations when removed. The 
Hirudo vorax is met with in parts of Europe and A frica. It gains 
access to the mucous membranes of the mouth, larynx, trachea, or 
nasal chambers, and leads to inflammatory troubles. It is not able 
to effect a lodgement upon the skin. 

ARTHROPODIA. 

A number of parasites belonging to the groups Arachnoidea 
and Insecta are met with in man. Most of these, however, are 
purely external parasites, and are fully described in works upon 
diseases of the skin. There are two forms, however, that merit 
brief description here : the Pentastomwn denticulatum, the larval 
form of Pentastomum taenioides ; and the larvae of various flies, 
the presence of which in the gastro-intestinal tract and other parts 
of the body is termed myiasis. 

PENTASTOMUM DENTICULATUM. 

This parasite is occasionally found in the liver and rarely in 
the spleen, intestinal walls, lungs, and kidneys of man. It is dis- 
covered in small nodular lesions, which consist of the more or less 
degenerated parasite lying in a cheesy or semicalcified material, 
surrounded by a fibrous or calcareous capsule. The parasite is 
from 4 to 5 mm. in length and 1.5 mm. in breadth ; has a rather 
rounded body, which is encircled by parallel rings armed with 
spicules ; and is provided with two pairs of stout chitinous hook- 
lets, one pair lying on either side of the mouth. The adult form, 
Pentastomum tamioides, resembles its larva in structure, but is 
considerably larger, the male being from 16 to 18 mm, long, the 
female from 60 to 85 mm. This form lodges in the nasal cavities 
and frontal sinuses of the dog and other animals, and produces 
eggs containing the embryos, which escape with the nasal secretion 
and eventually gain access to the alimentary tract of other animals 
or of man, 

MYIASIS. 

A number of flies, of the orders Estridae, Musca, Lucilia, and 
Sarcophaga, may deposit their eggs in wounds or in cavities of the 
body to which they gain access, such as the nasal or pharyngeal 
chambers and the communicating passages. The eggs so deposited 
are hatched, and the larval insects may be retained and may occa- 
sion intense irritation. Sometimes the larvae are found in the gas- 
tro-intestinal tract, the eggs having been swallow T ed with food. 
Immense numbers may be discharged from the intestines, and in 
some cases the larvae seem to occasion intestinal irritation. The 
term myiasis is given to the invasion of these larval insects. 



PART II. 
SPECIAL PATHOLOGY. 



CHAPTER I. 
DISEASES OF THE BLOOD. 
ANATOMY. 

The blood is a liquid tissue composed of corpuscles or cells 
and a fluid intercellular substance. The cells are of three kinds : 
the red corpuscles, or erythrocytes ; the white corpuscles, or leuko- 
cytes : and the blood-plaques, or hematoblcists. The fluid element 
of the blood, the liquor sangwinis, or plasma, is an albuminous and 
saline liquid of a slightly varying composition. The blood as a 
whole is red in color, rather viscid, and alkaline in reaction. The 
total quantity is about one-thirteenth of the body-weight. 

The erythrocytes, or red corpuscles, are biconcave disks 
about 7 ju in diameter and having a yellowish or amber color. 
They are quite uniform in size and regularly rounded. Histo- 
logically they are composed essentially of an albuminous substance 
containing hemoglobin embedded in a delicate stroma. The 
hemoglobin is the important element, and constitutes 95 per cent, 
by weight of the corpuscles. In early fetal life most of the red 
corpuscles are nucleated, but the nucleated forms later decrease in 
number and are comparatively scanty at the time of birth. 
Within the first few months of post-fetal life all of them dis- 
appear, and in subsequent years nucleated corpuscles are present 
only in cases of disease. 

There are about 5,000,000 corpuscles in the cubic millimeter 
of the blood of normal individuals. The figures vary slightly at 
different times in the same individual, and many influences con- 
tribute to the production of more lasting changes in number (see 
page 327). The volume of the red corpuscles in the blood is 
dependent upon the number of corpuscles and upon their size. 
Observers have reached varying results in studying the volume, 
but it may be placed at between 40 and 50 per cent, of the total 
bulk of the blood. 

The leukocytes, or white corpuscles, are rounded or 
spherical bodies presenting a more or less granular appearance in 

312 



DISEASES OF THE BLOOD, 



313 



the fresh state. They vary in size from the diameter of the red 
corpuscles to several times the size of the latter. The leukocytes 
are identical with the lymph-corpuscles. They are of several more 
or less distinct varieties ; the classification, however, is exceedingly 
difficult, as transitional forms are abundant. The classification 
most frequently adopted is that of Ehrlich and of his pupils, and 
while it is not entirely satisfactory, it has one advantage over 
others, viz., that of simplicity. Ehrlich distinguishes (Fig. 140) : 




Fig. 140.— Various forms of blood-corpuscles : a, lymphocyte ; b, lymphocyte approach- 
ing c; c, large mononuclear; d, transitional ; e, polymorphonuclear* neatrophile ; /, poly- 
morphonuclear eosinophile ; g, broken eosinophile ; h, neutrophilic myelocyte ; i, eosino- 
philous myelocyte ; j, basophile, mast-cell; k, red corpuscles ; I, nucleated red corpuscles. 

1. Small mononuclear leukocytes, or lymphocytes. These are 
smaller than the red corpuscles, or about the same size, are spher- 
ical, and contain a relatively large nucleus, the protoplasm often 
forming a scarcely visible band around the nucleus. The latter is 
rich in chromatin and stains deeply. Sometimes cells considerably 
larger than the typical lymphocyte may resemble them in other 
respects, and it may be difficult to determine whether these are 
lymphocytes or large mononuclear cells (Fig. 140, b). The proto- 
plasm of lymphocytes normally contains no granular matter when 
stained by the ordinary methods. Deep staining with methylene- 
blue with the aid of heat does, however, frequently lead to the 
detection of a slightly granular character in the protoplasm. 

2. Large mononuclear leukocytes. These forms are larger than 
the lymphocytes, being from two to three times the diameter of 
the red cells. They are often oval in outline, and the nucleus is 
poorer in chromatin than that of the lymphocyte, so that it appears 
comparatively pale in the stained blood. The protoplasm is 
usually free of granules, but it may show fine and very pale gran- 
ules when stained with intense basic stains like methylene-blue. 

3. Transitional leukocytes. These are similar to the last, but 



314 



TEXT-BOOK OF PATHOLOGY. 



differ in that the nucleus is often a little indented or horseshoe- 
shaped. It is very often impossible to determine satisfactorily 
whether a certain cell is a large mononuclear or a transitional 
form, and the two maybe considered as practically the same. The 
protoplasm, as a rule, contains no granules, but neutrophilic 
granules (see page 315) have occasionally been detected, and 
eosinophile granules are more frequently present. 

4. Polymorphonuclear leukocytes; polynuclear leukocytes; neu- 
trophiles. These are the most numerous forms, and probably 
represent the fully developed white blood-cell. They are some- 
what smaller than the large mononuclear elements, and are dis- 
tinguished by a polymorphous nucleus which is richer in chroma- 
tin than that of the large mononuclear form, though perhaps less 
rich than that of the lymphocyte. The nuclei are elongated, and 
variously curved or distorted so as to resemble the letters S, U, 
V, Z, etc., and in some cases they are wreath-shaped. Frequently 
parts of the nucleus are so thin that they are scarcely visible, or 
actually become broken, and the term polynuclear was therefore 
applied. This name is, however, less appropriate than the term 
polymorphonuclear. The amount of chromatin in the nucleus 
varies greatly, and the size of the nucleus is correspondingly 
variable. The protoplasm usually contains fine granules, which 
are closely set and almost completely fill the cell. These granules 
have a strong affinity for neutral mixtures of anilin or other stains, 
and have therefore been called the neutrophilic granules (see page 
315). A small proportion of the polymorphonuclear leukocytes 
of the blood contain eosinophile granules. These cells are usually 
larger than the neutrophilic forms, and the nucleus is more nearly 
like that of the typical transitional leukocyte. 

5. Myelocytes. These are large cells identical with the large 
granular cells of the bone-marrow. They are often three or 
four times the size of the red corpuscles, and are distinguished 
by a large, pale, oval nucleus. The protoplasm usually con- 
tains neutrophilic granules, but occasionally contains eosino- 
phile granules. The nucleus is frequently somewhat irregularly 
outlined and not rarely suffers degenerative change. Smaller cells, 
resembling the typical myelocyte in the character of the nucleus 
and protoplasm, are sometimes observed, and are difficult to clas- 
sify. Myelocytes occur in exceedingly small numbers, if at all, 
in normal blood. They are abundant in certain forms of leukemia, 
and also occur in pernicious anemia and various infectious and 
systemic diseases. 

The granules of the leukocytes are classified according to their 
behavior with the anilin stains. We may distinguish four impor- 
tant types of granules (Figs. 140 and 141) : 

1. a-granules, eosinophile granules, or oxyphile granules. These 
are coarse granules giving the appearance in the unstained blood 



DISEASES OF THE BLOOD. 



315 



of minute fat-droplets ; they are highly refractive, and have been 
shown to be composed of albuminous material. They are dis- 
tinguished by their strong affinity for acid stains/ and in particular 
for eosin. This circumstance has given rise to the name eosino- 
phil and oxyphile (Fig. 147). 

The eosinophile granules in the normal blood occur only in 
polymorphonuclear leukocytes. 

2. y-granules ; mast-cell granules. These are intensely baso- 




c 

d 



Fig. 141. — Leukocytes, showing various forms of granulations : a, Neusser's basophilic, 
perinuclear granules ; b, large mononuclear cells with 6-granules ; c, mast-cell granules . 
d, basophilic lymphocytes, 5-granules ; the stain in b, c, and d was a mixture of eosin and 
hematoxylin, the cover-glass being kept in the stain several hours at 37° C. (98.6° F.). 

philicj coarse granules, occurring in mononuclear cells. The mast- 
cell is identical with Waldeyer's plasma-cell of the tissues. It is 
present in small proportions in the normal blood (Fig. 141). 

3. o-granules are fine basophilic granules occurring in the 
lymphocytes or large mononuclear cells (Fig. 141). 

4. e-granules ; neutrophilic granules. These are the most abun- 
dant and the most important of all the forms. They occur as 
fine granulations filling up the protoplasm of the polymorphous 

1 The term acid stain is here used in a sense somewhat different from that of 
the chemist. A stain in which the acidulous part of the compound carries the 
coloring-principle is known as an acid stain, while one in which the basic ele- 
ment is the staining-principle is called basic. For example : picrate of am- 
monium is an acid stain because the picric acid is the staining-element. Mixt- 
ures of certain acid with basic stains may be prepared so that tissue-elements 
having a strong acid affinity will select the acid stain, those having a basic affinity 
the basic stain, while other elements without such special affinity receive a mixed 
or neutral stain. It is probably more correct to regard the neutrophile-mixtures 
as weakly oxyphile. 



316 



TEXT-BOOK OF PATHOLOGY. 



cells, and they are occasionally present in transitional leukocytes. 
They are distinguished by their affinity for the neutral mixtures 
of Ehrlich (Fig. 147). It must be recognized, however, that these 
granules are in reality faintly oxyphilic, receiving the acid stains, 
such as eosin or acid fuchsin, more readily than basic stains. In 
a few instances I have found them distinctly basophilic. 

The nature of the granules of the blood is still obscure. They 
are undoubtedly connected in some way with the specific function 
of the leukocytes, but whether they are specific cellular secretions 
(Ehrlich) or essential anatomical structures (Altmann) is unknown. 

The chemical composition of the leukocytes is of considerable 
importance, but is difficult to determine from the impossibility of 
obtaining large numbers free from other elements. It is known, 
however, that these cells contain among other bodies leukonuclein, 
histon, lecithin, and cholesterin. They also contain more or less 
abundantly glycogen and fats ; and saline constituents including 
potassium salts in particular. The leukonuclein is a combination 
of the phosphorus-containing nucleinic acid and an albumin. It 
is present in the nuclei of nucleated red corpuscles and in other 
nuclei, but especially in those of the leukocytes. It is more or 
less intimately combined with histon, a body resembling the albu- 
moses. 

The number of leukocytes in the normal blood varies consider- 
ably. The average number, however, is probably between 6000 
and 10,000. Alterations in the number under various circum- 
stances will be discussed below. 

Proportions of the Different Forms. — The relative proportions 
(" differentia] count ") of the different leukocytes are determined 
by counting large numbers and calculating the percentage propor- 
tion of each form. Approximately there are 25 per cent, lympho- 
cytes, 65 to 75 per cent, polymorphonuclear forms (neutrophiles 
and eosinophiles), 5 to 8 per cent, transitional and large mononu- 
clear. ' About 1 to 3 or 5 per cent, of all the leukocytes contain 
eosinophile granules, and occasionally a larger porportion is met 
with in normal blood. 

Blood-plaques. — These are small disks somewhat resem- 
bling the red corpuscles, though smaller and without the charac- 
teristic biconcavity of the latter. They rarely exceed 3 p. in 
diameter, and are often much less. They are viscid, and tend to 
adhere to the other corpuscles or to become agglutinated in clusters. 
The total number has been estimated at from 150,000 to 500,000 
per cubic millimeter. The term hematoblast was applied by 
Hayem in the belief that the plaques are the progenitors of the 
red corpuscles. Recent investigations make it seem probable that 
the plaques are formed by fragmentations of the red corpuscles. 

The plasma of the blood is an albuminous liquid containing 
serum-albumin and serum-globulin and various saline compounds. 



DISEASES OF THE BLOOD. 



317 



The relative proportion of serum-globulin to serum-albumin is as 
1 to 1 or \\. Of the saline constituents sodium salts are most 
important, the phosphates, carbonates, sulphates, and chlorids 
being most abundant. Various other nitrogenous and non-nitro- 
genous substances are present in small proportions. Reference 
will be made to some of these below. 

BLOOD=FORMATION. 

The process of blood-formation is still obscure in some particu- 
lars. In early fetal life blood-corpuscles are undoubtedly formed 
in the mesoblastic columns in which the blood-vessels are devel- 
oped. At a later stage the liver is active in their production. 
Subsequently the spleen and the bone-marrow seem to assume the 
principal role. According to Neumann and Bizzozero, the red 
corpuscles are developed from nucleated hemoglobin-containing 
cells of the bone-marrow, which lose their nuclei by a process of 
gradual disintegration. Others have held that the nuclei are ex- 
truded from the nucleated celL According to these views, all of 
the red corpuscles are derived from nucleated red cells, or eryth- 
roblasts. Other observers, however, hold that the red corpuscles 
and leukocytes originate from a common parent-cell free from 
hemoglobin. This parent-cell gives rise to two series of descend- 
ants, one series containing hemoglobin and leading to the formation 
of red corpuscles, while the other series is free from pigment and 
forms the leukocytes. The principal place of formation of the 
red corpuscles during adult life seems to be the bone-marrow, but 
the spleen and the lymphatic tissues probably also play a part. 
French writers, following Hayem, hold that the progenitor of the 
red corpuscle is the blood-plaque. This view, however, is not 
sustained by sufficient evidence. 

The white corpuscles undoubtedly originate in the bone-marrow, 
lymphatic tissues, and spleen. The lymphocyte is the youngest 
form, and the other varieties probably are secondary developments 
from this, the completion of their development occurring in the 
blood-making organs, notably the marrow. 

PATHOLOGIC CHANGES IN THE RED CORPUSCLES. 

The sise of the red corpuscles varies in diseases of different 
kinds. There may be dwarf corpuscles, 2 to 4 or 5 {/. in diameter 
(mierocytes) ; or, on the other baud, giant-cells (megalocytes), from 
9 to 15 [i or even 20 fi in diameter. The small forms frequently 
have a spherical shape rather than the disk-like form of the nor- 
mal corpuscle, and may be deeply pigmented. The large corpus- 
cles are often irregular in shape, and are prone to be paler than 
normal corpuscles (Fig. 142). Some observers have found that 
the average size of the red corpuscle is greater in certain diseases 
than in health. This is probably the result of hydropic conditions. 



318 



TEXT-BOOK OF PATHOLOGY. 



The shape of the corpuscles often suffers great change, and 
many forms of irregularity may be observed. The term poikilocy- 
tosis is applied to this condition (Fig. 142). Some of the poikilo- 
cytes may be exceedingly small and may present active movements. 
These have been termed pseudobacilli by Hayem. These changes 
of form in red corpuscles are regarded by many authorities to be 




Fig. 142.— Blood from a case of pernicious anemia : a, megalocytes ; b, microcytes ; c, poi= 
kilocytes ; d, nucleated erythrocytes ; e, normal erythrocytes ; /, leukocytes. 

the result of degenerative changes in the protoplasm with conse- 
quent ameboid movement Avhich occasions irregular projections. 
The small forms are doubtless in many cases the result of frag- 
mentation. Ehrlich used the term schistocyte to indicate this fact. 

Dust-corpuscles. — Miiller recently described certain small 
spherical bodies somewhat resembling the leukocytic granules, but 
lying free in the plasma and often actively motile. These he 
termed hemokonice, or dust-corpuscles. They occur in normal blood 
as well as in that of various diseases. A number of theories have 
been offered regarding the nature of these bodies. My own belief 
is that they are fragments of red corpuscles, similar to those that 
may be produced by heating fresh blood under a cover-glass to 
destructive temperatures. Under these circumstances small, bud- 
like processes are formed on the periphery of the red corpuscles, 
and some of these may break off and float free in the plasma. 

Visible ameboid movemeuts may sometimes be observed 
under the microscope, especially in severe anemias, such as per- 
nicious anemia. 

Nucleated red corpuscles, or erythroblasts, occur in the 
severe anemias as in the fetal blood. They are more frequent in 
the severest cases, and in particular in the anemias of children. 
Some are exceedingly small (microb lasts), some about the size of 
the normal red corpuscle (normoblasts), and some large and irregu- 
lar (meg alob lasts). The smaller forms appear first and in the more 



DISEASES OF THE BLOOD. 



319 



moderate anemias ; occasionally they occur in great numbers or 
crops from time to time (blood-crises). 

Karyokinetic figures are occasionally seen in the nuclei of 
erythroblasts, especially in certain anemias of children. 

Shadow corpuscles are red corpuscles that have lost their 
color almost completely and are scarcely visible. They may be 
observed in severe anemias, and especially in cases of intoxication 
with blood-poisons. 

Polychrotnatophilia. — The normal red corpuscle has a spe- 
cial affinity for acid stains. In diseased conditions it may develop 
an affinity for basic stains, and when colored with mixtures of acid 
and basic stains may present tints combining all the stains employed. 
Thus in staining with eosin and hematoxylin the degenerated 
corpuscles may present a purplish or violet color, instead of a 
pink. 

Vacuolation and pigmentation of the red corpuscles are 
rare forms of degeneration. The pigmentation is due to separa- 
tion of the hemoglobin in the form of irregular granules. 

Alterations of Isotonicity. — All forms of cells have cer- 
tain osmotic relations, in consequence of which they retain their 
constituent elements in the presence of surrounding liquids of 
certain kinds. If the osmotic relations vary or the surrounding 
liquids are altered, the constituents of the cell may be extruded. 
In the case of blood-corpuscles distilled water rapidly abstracts 
the hemoglobin and other substances, but saline solutions of cer- 
tain strengths do not so affect the corpuscle. The exact strength 
of a certain saline solution may be determined which will preserve 
the corpuscle, and this is known as the isotonic strength of the 
corpuscle expressed in percentage-terms of the saline used. De- 
generated corpuscles more readily yield their constituents, and the 
isotonic saline solution is therefore of higher percentage. In 
normal blood the isotonicity of the red corpuscle is generally 0.46 
to 0.48 per cent. NaCl ; that is, solutions of common salt of this 
strength do not affect the red corpuscles. In anemic diseases the 
isotonic solutions may be from 0.5 to 0.6 per cent. 

PATHOLOGIC CHANGES IN THE LEUKOCYTES. 

Very frequently degenerations of the nuclei of the leukocytes 
are observed in the form of fragmentations or karyolytic change. 
Attention has recently been called (Neusser) to the presence of 
basophilic granules about the nucleus in certain forms of disease, 
such as leukemia, gout, and lithemia in its widest sense. These 
granules are supposed to be significant of disintegration of the 
nuclei in the process of uric-acid formation. Their nature and 
significance, however, are unsettled. Occasionally vacuolization 
and fatty degeneration of leukocytes are observed, and sometimes, 
,as in infectious fevers and in suppuration, glycogen may be found 



320 



TEXT-BOOK OF PATHOLOGY. 



in abnormal quantities. In cover-glass preparations the leuko- 
cytes are sometimes found broken or fragmented, and this doubt- 
less occurs to some extent in the circulating blood. 

PATHOLOGIC CHANGES IN THE PLASMA. 

Various disorders of the plasma have been studied. These are 
mainly of a chemical sort, and consist of the presence of abnormal 
substances or of normal constituents in excessive quantity. Urea 
is present in large quantities in some cases of nephritis and uremia, 
and older authorities believed the symptoms of uremia due to the 
presence of this substance. This view is no longer held. Uric 
acid occurs in small quantities in health ; but in large quantities 
in gout, leukemia, leukocytosis, and other disorders of the blood. 
The xanthin bases may be present in considerable quantities in the 
same cases. Glycogen or grape-sugar is found in excessive quan- 
tities in diabetes and, according to some observations, in cases of 
carcinoma. Levulose and other carbohydrates are rare constitu- 
ents of the plasma. Fatty acids may be present in leukemia, dia- 
betes, acute yellow atrophy of the liver, and some other diseases. 
The quantity of sodium in the plasma increases in anemic diseases. 

Certain changes occur in the plasma or serum in anemic dis- 
eases, as a result of which the globulicidal character is increased. 
The nature of these changes is obscure. The presence of toxic 
substances the result of bacterial action is referred to in the dis- 
cussion of bacteria. 

Hype /tonicity of the serum is a term indicating that the salinity 
of the plasma or serum is such that the blood may be somewhat 
diluted without destruction of the corpuscles. By graduated dilu- 
tions the degree of hypertonicity may be estimated, and is found 
less in certain diseases than in health (see Isotonicity of the Red 
Corpuscles). 

Hyperiuosis and hyjnnosis are terms designating increased and 
decreased capability for fibrin-formation. The former is met with 
at times in chlorosis, leukemia, or other anemic affections, and in 
certain infectious diseases. The latter is notably present in leu- 
kemia and some cases of hemolysis. There has been much the- 
orizing in regard to these conditions, but very little knowledge of 
practical importance has been acquired. 

PLETHORA. 

Plethora is the name applied by the older writers to a condition 
in which the total quantity of blood was supposed to be excessive. 
It is now recognized that plethora is much less frequent and per- 
manent than was formerly believed. Several varieties were de- 
scribed. 

Plethora vera was the name given to the condition in which 
the quantity of the blood was supposed to be increased without 



DISEASES OF THE BLOOD. 



321 



change in its quality. Persons supposed to have this condition 
are described as robust, with high color and vigorous circulation. 
They are generally individuals living in luxury. The term " full- 
blooded " is still applied, but it is recognized that the fulness of 
the superficial vessels is the result of peculiarities of the circulation 
rather than of increase in the quantity of blood. 

Plethora apocoptica is the term given to conditions in 
which there is local increase in the blood. 

Plethora hydremica is a condition in which the total quan- 
tity of the blood is increased by dilution. This was regarded as 
frequent in cases of cachexia, after hemorrhages, etc. 

Experimental evidence might be referred to to substantiate the 
view that plethora in the strict sense does not often occur as a 
lasting condition. Temporary plethora is produced by the drink- 
ing of large quantities of liquid, but the excretory organs soon 
dispose of this excess. 

OLIGEMIA. 

Oligemia is a term indicating reduction in the quantity of blood. 
This is met with temporarily after hemorrhage, but very soon 
serous liquid from the tissues enters the blood-vessels and restores 
the original quantity. At the time of the hemorrhage the quantity 
may be immediately reduced to a very great degree without caus- 
ing death. Serious consequences are averted by the activity of 
the vasomotor system, the blood-vessels accommodating them- 
selves by contraction to the reduced quantity of blood. Subse- 
quently when liquid of the tissues is absorbed into the blood- 
vessels the latter dilate and their natural volume is soon restored. 
The blood, however, becomes hydremic, or watery. Oligemia or 
quantitative anemia may possibly occur in certain cachectic and 
anemic diseases, but this has not been proved, and the relative 
proportion between the mass of blood and the weight of the body 
is certainly not much disturbed in any case. 

HYDREMIA AND ANHYDREMIA. 

Hydremia, a diluted or watery condition of the blood, may 
occur from excessive consumption of water, but active excretion 
of liquid soon restores the blood to its previous condition. Hemor- 
rhage leads to hydremia in the manner above described ; and in 
the chronic anemias there is possibly some dilution of the serum. 
It has never been shown, however, in any of the many experiments 
made to determine this point, that the plasma in anemias is less 
rich in solid constituents than normal plasma. The reduction in 
solid matter in the blood as a whole is due to the diminution in 
the number of red corpuscles and changes in their composition. 

Anhydremia is a condition in which the plasma of the blood 

21 



322 



TEXT-BOOK OF PATHOLOGY. 



is thickened by the loss of watery elements. This may occur in 
consequence of excessive sweating or excessive discharge of water 
from the bowels, kidneys, etc. The number of red corpuscles in 
a given bulk of blood increases. The specific gravity and the 
solid residue of the plasma of the blood as a whole increase corre- 
spondingly. 

LIPEMIA. 

Lipemia is a pathologic condition in which fat occurs free in 
the blood-plasma. Fat is always present as a normal constituent 
of blood, and is in slight excess during the process of digestion. 
Lipemia occurs in cases of chronic nephritis, diabetes, pulmonary 
tuberculosis, alcoholism, and some other conditions, and may reach 
marked grades of severity. The blood may have a milky appear- 




Fig. 143.— Blood from a case of lipemia, stained with osmic acid: tipper half of field 
cleared with oil of turpentine; lower half shows the fat-droplets and granules stained 
with osmic acid between the blood-corpuscles ; enlargement, 100 diameters (after Gum- 
precht; Deutsch med Woch., Sept. 27, 1894). 



ance to the naked eye, and under the microscope highly refractive 
droplets or granules are observed. The latter stain black with 
osmic acid (Fig. 143). 



MELANEMIA. 

This condition is distinguished by the occurrence of dark pig- 
ment or granular matter in the circulating blood. It occurs in 
cases of malaria and certain other fevers. The pigment may be 



DISEASES OF THE BLOOD. 



323 



free in the plasma in the form of yellowish or blackish granules ; 
or may be found as small particles in the leukocytes. 

HEMOCYTOLYSIS— HEMOGLOBINEMI A. 

Definition. — Hemocytolysis is the term applied to the condi- 
tions in which the red blood-corpuscles are destroyed. The name 
hemolysis is generally employed in the same sense, though it refers 
to destruction of all of the elements of the blood. In this condi- 
tion hemoglobin is liberated and is dissolved in the plasma. To 
this the term hemoglobinemia is applicable, but the name met- 
hemoglobinemia is more appropriate, as the hemoglobin is usually 
present in the serum in this altered form. 

Etiology. — Hemolysis constantly takes place in the liver, the 
coloring-matter of the blood being converted into bile-pigments. 
Pathologic hemolysis results from the action of various infectious 
and toxic agents. It occurs in the course of severe malaria, re- 
lapsing fever, pneumonia, and various hemorrhagic infections ; and 
is occasioned by many poisons (see Blood-poisons). Excessive 
cold may be a contributing cause, as seems to be the case in some 
instances of paroxysmal hemoglobinuria {q. v.). 

Pathologic Anatomy.— The blood may present striking 
morphologic changes in the red corpuscles, such as microcyto- 
sis, megalocytosis, )poikilocytosis, fragmentation, and vacuolation. 
Shadow-corpuscles may be abundant, and in the later stages of 
the process beginning regeneration of the blood causes the pres- 
ence of nucleated red corpuscles. The blood as a whole is often 
quite dark in color. 

Associated changes are frequently met with in the liver, kid- 
neys, and skin. The hepatic cells are often swollen and more or 
less degenerated and bile-stained. Excessive production of bile 
(polycholia) may occur. This over-production, with the swelling 
of the hepatic cells and the consequent obstruction of the biliary 
channels, occasions reabsorption of bile and consequent jaundice 
(so-called hematogenous jaundice). The excess of hemoglobin, 
which cannot be disposed of by the liver, may be excreted in the 
urine (hemoglobinuria). Sometimes hemoglobin-infarcts are met 
with in the renal tubules ; and thrombosis of the renal or other blood- 
vessels is occasionally observed. Acute nephritis is a rare result. 

Pathologic Physiology. — Hemocytolysis leads to more or 
less pronounced disturbance of the internal or tissue respiration, 
as the altered hemoglobin is incapable of carrying oxygen. Dysp- 
nea and various nervous symptoms are the result. The liberation 
of cellular constituents (from destruction of the red and white 
corpuscles) occasions increased coagulability of the blood and the 
formation of thrombi (ferment-intoxication). Fever and other 
general symptoms may be due to the same cause. 



324 



TEXT-BOOK OF PATHOLOGY. 



POLYCYTHEMIA. 

Polycythemia, or erythrocytosis, the condition in which the num- 
ber of red corpuscles in a given bulk of blood is increased, may be 
actual or relative. Actual polycythemia is that in which there is 
over-production of red corpuscles ; this is probably rare. Relative 
polycythemia is due to decrease in the quantity of the plasma. It 
is met with in a variety of conditions, including certain cardiac 
diseases, with slow failure of compensation, and especially in con- 
genital cyanosis ; in residents of high altitudes ; in the new-born ; 
and in cases of cholera or other diseases in which liquid discharges 
cause inspissation of the blood. The explanation of the increased 
number of corpuscles in some of these conditions has occasioned 
considerable controversy. Some have held that the number of 
corpuscles (at high altitudes, for example) increases actually rather 
than relatively, for the purpose of furnishing a greater oxidizing 
surface, but this has not been proved. It is more likely that the 
increased number of corpuscles is caused by changes in their dis- 
tribution in the circulation. In evidence of this it maybe pointed 
out that the number of corpuscles in dependent parts, such as the 
foot, is greater than normal. In cardiac disease and in persons 
living at high altitudes it is not improbable that similar stagnation 
of the corpuscles in the peripheral tissues takes place. 

LEUKOCYTOSIS. 

The term leukocytosis is given to a more or less transient in- 
crease in the number of leukocytes, the polymorphonuclear forms 
being usually in excess. Sometimes leukocytosis is continuous or 
chronic, and sometimes the excessive number of leukocytes is due 
to increase in the mononuclear elements rather than the polymor- 
phonuclear. 

Etiology. — The causes of leukocytosis are varied. It is 
generally observed as a normal condition in the new-born, the 
number of corpuscles remaining in slight excess during the first 
year of life. It also occurs in many cases of pregnancy ; and is 
quite constant during the period of digestion in healthy persons, 
proteid food being more striking in the effect than a farinaceous 
or mixed diet. In some diseases of the stomach post-digestive 
leukocytosis seems not to occur. 

Inflammatory and Infectious Leukocytosis. — Among the strictly 
pathologic forms of leukocytosis the most important are those due 
to inflammations and infections of various kinds. Croupous 
pneumonia occasions considerable increase of leukocytes in most 
cases, and this is continuous until the final decline of the fever. 
Suppurations of all kinds act in a similar manner. Inflammations 
of the serous membranes — peritonitis, pleurisy, meningitis — may 



DISEASES OF THE BLOOD. 



325 



be attended by moderate or severe leukocytosis. Among the acute 
infectious fevers there are some in which leukocytosis occurs and 
others in which this is wanting, and this fact often proves valu- 
able to the clinician. Among those in which the leukocytes do 
not increase in number are typhoid fever, influenza, malaria, and 
acute miliary tuberculosis. 

Cachectic leukocytosis occurs in a variety of marantic conditions, 
and toward the end of life in any case of wasting disease there may 
be a great increase in the number of leukocytes. This agonal 
or terminal leukocytosis is either cachectic (toxic) in nature or it 
may be due to terminal infections. 

Malignant tumors frequently cause leukocytosis. 

Hemorrhage may occasion increase in number of the white cor- 
puscles, more or less in accordance with the quantity of blood lost. 

Mechanical and Thermal Causes. — Massage and cold baths fre- 
quently cause increase in the number of leukocytes for a time. 

Medicinal leukocytosis, or that due to the introduction of various 
drugs, is probably allied to infectious and cachectic leukocytosis 
in the manner of its production. 

Pathogenesis. — The nature of leukocytosis is still the sub- 
ject of some controversy. Formerly it was held that the in- 
creased number of leukocytes is wholly due to overproduction ; 
later, some investigators claimed that diminished destruction is the 
important cause. The explanation which seems most acceptable 
at the present day is that of Goldscheider and Jakob. These 
observers hold that infectious and toxic leukocytosis is due to the 
attractive influence of the toxic substances upon the leukocytes in 
the blood-making organs, and to a certain extent to the stimu- 
lating influence upon those organs, leading to increased production 
of leukocytes. There are at all times large numbers of leuko- 
cytes in the lymphatic tissues and throughout the other tissues of 
the body which may be drawn into the circulation by chemotactic 
substances. AVhen, however, leukocytosis is prolonged it is likely 
that new-formation of leukocytes takes place, as the supply would 
otherwise soon become exhausted. 

Character of the Blood. — The blood in leukocytosis varies 
considerably in character. The number of leukocytes may be 
only moderatelv increased (10,000 to 20,000) or may be excessive 
(50,000 to 100,000). The older writers distinguished between 
leukocytosis and leukemia by the number of leukocytes present. 
This distinction is no longer admitted, as there are cases of leuko- 
cytosis with very marked increase in the number of the leuko- 
cytes and cases of leukemia with leukocytosis temporarily or con- 
tinuously of more moderate degree. 

In the majority of cases of leukocytosis the polymorphonuclear 
elements are in relative as well as actual excess, the mononuclear 
elements being actually increased in number, but relatively defi- 



326 



TEXT-BOOK OF PATHOLOGY. 



cient (Fig. 144). The proportion of polymorphonuclear elements 
is frequently 80 to 85 per cent., and sometimes 90 or 95 per cent., 
instead of 65 to 70 per cent. In the leukocytosis of the new-born, 
in hemorrhagic leukocytosis, cachectic leukocytosis, and that due 




Fig. 144.— Septic leukocytosis, showing marked increase of polymorphonuclear leukocytes. 

to malignant tumors, the mononuclear elements frequently pre- 
ponderate. Occasionally myelocytes have been observed, and 
karyokinetic figures may occur in the nuclei. 

Pathologic Physiology. — Leukocytosis certainly exercises 
some profound influence upon the system, but the exact nature of 
this influence is unsettled. Those who contend in favor of the 
phagocytic theory of immunity claim, more or less directly, that 
the increase of leukocytes is a protective process, the purpose 
being the removal and destruction of irritants. Others believe 
that leukocytosis is part of the cellular processes concerned in the 
production of immunizing substances. There is certainly more 
active destruction of leukocytes in leukocytosis than in health, as 
is evidenced by the increase of xanthin bases and uric acid in the 
urine ; and it may be that in this destruction protective substances 
are liberated. 

HYPOLEUKOCYTOSIS. 

Hypoleukocytosis, or leukopenia, is the condition in which there 
is deficiency in the number of leukocytes. This is met with in 
moderate degree in various diseases, such as tuberculosis, typhoid 
fever, some cases of pneumonia, cachexia, inanition, progressive 
pernicious anemia, etc. The nature of hypoleukocytosis is not 
always clear. Some have held that it is due to destruction of 
leukocytes (leulcolysis), while others claim that it is the result of 
altered distribution of the leukocytes. It has been shown by 
experimenters that the injection of certain micro-organisms or 
toxic substances will produce, first, a decrease in the number of 



DISEASES OF THE BLOOD. 



327 



leukocytes, and then an increase. The primary hvpoleukocytosis 
is explained by some as the result of active destruction of leuko- 
cytes, but the conditions of the urine do not give evidence of such 
active destruction, and others have shown that the capillaries of 
the lungs, liver, and other organs are overfilled with leukocytes 
during this stage. The assumption is therefore warranted that 
hvpoleukocytosis is the result of disturbance in the distribution of 
the leukocytes. 

ANEMIA. 

Definition. — This term includes a variety of conditions in 
which the blood is reduced in quality in one direction or another. 
The term oligocythemia indicates a reduction in the number of red 
corpuscles, while the name oligochromemia indicates a reduction in 
the coloring-matter of the corpuscles. Usually these conditions 
are associated. 

Classification of Anemias. — It is not as yet possible to 
offer a strictly scientific classification, but for ordinary purposes the 
old division into primary and secondary anemias may be retained. 
The term primary anemia may be given to forms in which 
the anemia is the striking pathologic condition. The older 
writers used the name to indicate that the anemia was an essen- 
tial disease and dependent upon no preceding affection, excepting 
possibly a disturbance of the hematopoietic organs. The term 
secondary anemia, or symptomatic anemia, may be used to desig- 
nate anemic conditions in which some underlying disease that has 
occasioned the anemia is conspicuous. According to the classi- 
fication here offered, all anemias are recognized as secondary in 
the strict sense, but those in which the underlying disease is not 
conspicuous are classified as primary, and those in which the origi- 
nal disease is conspicuous as secondary. 

SECONDARY ANEMIA. 

Etiology. — Various unsanitary conditions may influence the 
character of the blood by the constant disturbance of the organic 
functions. A cause of immediate anemia is hemorrhage. This 
first leads to reduction in the quantity of blood ; and later by 
absorption of liquid from the tissues to dilution of the blood, or 
hydremia. Finally, after a variable period the character of the 
blood is restored by regeneration of corpuscles and of coloring- 
matter. Parasites of various sorts may lead to anemia. Among 
the more important are the intestinal worms, Anchylostoma 
duodenale, Bothriocephalus latus, and Anguillula intestinalis. The 
mode of action of these is not entirely clear. Some have held 
that they cause anemia by loss of blood through the intestine, and 
this is probably true in the case of Anguillula, but marked anemia 



328 



TEXT-BOOK OF PATHOLOGY. 



may occur from the presence of Bothriocephalus or Anchylostoma 
without much hemorrhage taking place. An explanation worthy 
of consideration in these cases is that the parasites generate 
poisons either in their ordinary life or by their death and decom- 
position, and that these poisons are the cause of the anemia. 
Other intestinal parasites may occasion more or less anemia 
directly or indirectly. The parasites occurring in the blood itself, 
notably the malarial organism, may cause extreme anemia. Infec- 
tious diseases frequently lead to impoverishment of the blood. In 
the acute febrile diseases, such as typhoid fever, rheumatism, and 
pneumonia, the anemia may not be conspicuous during the prog- 
ress of the disease, but becomes apparent after the fever has sub- 
sided. This may be explained by the assumption that increased 
respiration and sweating cause inspissation of the blood and 
relative increase in the number of red corpuscles during the exist- 
ence of fever, so that the anemia is unnoticed. In chronic infec- 
tions, such as syphilis and tuberculosis, marked anemia may occur. 
Among the poisons capable of producing anemia are lead, arsenic, 
phosphorus, and the like, and experimentally pyrogallol, nitro- 
benzol, and similar substances have been used to produce anemia. 
The anemias of various infectious diseases are undoubtedly toxic in 
character, and very probably those occurring in gastro-intestinal 
and nutritional diseases are similarly the result of the action of 
poisons generated within the body. Organic diseases and new 
growths of various sorts may occasion anemia by the general dis- 
turbance of health, by toxic products generated in the course of 
disease, by hemorrhage, etc. 

Pathologic Anatomy. — The condition of the blood in sec- 
ondary anemias varies with the duration and grade of the anemia. 
In moderate cases the number of red corpuscles decreases slightly 
(4,000,000 to 3,000,000), and the hemoglobin is correspondingly 
reduced, though often somewhat more strikingly than the corpus- 
cles. The fresh blood may show no visible changes under the 
microscope, and even in stained preparations the appearance may 
be normal. More marked anemia is distinguished by greater re- 
duction, the number of corpuscles sinking to 2,500,000 or 2,000,000 
per cu.mm. in extreme cases. The hemoglobin is usually reduced 
more markedly than the corpuscles. Examination of the fresh 
blood shows pallor of the corpuscles and various irregularities in 
size (microcytes and megalocytes) and shape (poikilocytes). Nu- 
cleated red corpuscles may be present in small numbers, the 
microblasts and normoblasts predominating. The stained blood 
may disclose degeneration of the corpuscles by the presence of 
polychromatophilic forms. The leukocytes do not play an essen- 
tial part in this form of anemia. Their number may be normal 
or reduced ; in other cases leukocytosis is present. The relative 
proportions of the different forms is usually about normal. In 



DISEASES OF THE BLOOD. 



329 



severe cases the lymphocytes may increase relatively and actually , 
at the expense of the polymorphonuclear forms. Myelocytes are 
occasionally present. 

Associated changes in various organs may be met with. Among 
these are parenchymatous and fatty degeneration of the heart, 
kidneys, and liver. These conditions have often been ascribed to 
reduced oxidation, which was supposed to be due to poverty in he- 
moglobin. Physiologic studies, however, do not establish the ex- 
istence of a reduction in the respiratory exchange of gases. It is 
likely that toxic conditions of the blood occur in anemia, and that 
the poisons act directly upon the affected organs. 

Pathologic Physiology. — The process of oxidation is of 
particular interest in anemia, and, as has been stated, recent in- 
vestigations show that the consumption of oxygen and elimination 
of carbon dioxid are normal. To accomplish this result more 
active circulation and greater energy of the tissues are required. 
Partly in consequence of the latter, diseases of the organs named 
in the last paragraph result ; and at the same time some of the 
characteristic symptoms (palpitations, dyspnea) are produced. In 
severe secondary anemias increased tissue- waste occurs, and nitro- 
gen is discharged in excess of that ingested. 

THE PRIMARY ANEMIAS. 

The conditions included under this title are chlorosis, progres- 
sive pernicious anemia, leukemia, and Hodgkin's disease. The 
term simple primary anemia is sometimes used to designate a form 
of anemia without distinct cause, and characterized by moderate 
oligocythemia. There are, it is true, occasional cases of moderate 
anemia in which no definite precedent disease can be discovered ; 
but these are exceptional cases, and are to be considered as sec- 
ondary anemias in which the underlying disease is latent. Cases 
of this sort do not conform to a definite type, and cannot there- 
fore be considered as illustrating a special form of anemia. 
Another term frequently used is splenic anemia. This is even 
less satisfactorily defined. Splenic enlargement may occur in 
any of the primary anemias, and may in some cases be excessive. 
Moreover, some of the distinctly secondary anemias (as those of 
rickets, syphilis, and malaria) are very often attended with splenic 
enlargement. It has not been proved that there is a special form 
of anemia with splenic enlargement as the conspicuous lesion, and 
cases of so-called splenic anemia are to be considered as secondary 
or primary anemias in which splenic enlargement happens to be 
marked. 

CHLOROSIS. 

Definition. — Chlorosis is a primary anemia due to retarded 
hemogenesis, characterized by a peculiar pallor and marked reduc- 



330 



TEXT-BOOK OF PATHOLOGY. 



tion in the percentage of hemoglobin, and occurring almost exclu- 
sively in young girls and women. 

Etiology. — Chlorosis is most frequent at the time of begin- 
ning menstruation and during the years immediately following 
this. A form of late chlorosis has been described in women above 
thirty years of age and at the menopause ; but the nature of this is 
doubtful. Chlorosis in the male is still more doubtful, though a few 
cases have been described by competent observers. Hereditary 
tendencies are of etiologic importance. The disease occurs more 
frequently in families in which tuberculosis is common than in 
those not so affected. Constitutional predisposition is also an 
important factor, poorly developed girls, and particularly those of 
delicate mould, being especially liable to the disease. Virchow 
found hypoplasia of the heart and great vessels, and Rokitansky 
the same condition in the generative organs, and pathologists 
have been inclined to regard these as important factors in the 
development of the disease. 

Various exciting causes have been considered as of more or less 
importance. Emotional excitement was regarded as a prime cause 
by ancient authorities, and in consequence such terms as icterus 
seufebris amantium were applied. Home-sickness, grief, etc., are 
causes of moment. Intestinal auto-intoxication has been regarded 
as the essential factor by many, but physiologic chemists fail to 
find evidences of the existence of such intoxication. Menstrual 
disturbances are important as symptoms, and have often been re- 
garded as causes. The hypoplasia of the genital organs adds some 
probability to this view, but more definite evidence is wanting. 

At the present time it seems most likely that chlorosis is due 
to faulty development, and especially to a want of proper hemo- 
genetic power. 

Pathologic Anatomy. — The hypoplasia of the vascular and 
generative systems has been referred to. These are primary 
lesions, and possibly causal. Various secondary diseases may be 
encountered, as in other anemias. Among these, myocardiac de- 
generation and dilatation are most important, though they do not 
attain high grades of severity. The spleen is frequently a little 
enlarged. Peculiar yellowish or greenish pigmentation of the 
skin is a striking feature. The pigment is doubtless altered 
hemoglobin, but its exact nature is unknown. 

The Blood. — The blood is paler than normal, and watery. The 
specific gravity decreases progressively, and the solid matter 
is deficient. Increased coagulability is sometimes observed. The 
number of red corpuscles may be normal, even in well-developed 
cases, but the proportion of hemoglobin sinks progressively. 
In prolonged cases the corpuscles become reduced in number, 
but the deficiency of hemoglobin continues to be excessive. 
Severe cases of chlorosis frequently show 3,000,000 or 2,000,000 



DISEASES OF THE BLOOD. 



331 



red corpuscles per cu.mm. and 30 per cent, to 20 per cent, of 
hemoglobin. The red corpuscles may be little altered in ap- 
pearance in the early stages ; later, irregularities in size and 
shape are frequent, and nucleated red corpuscles (especially small 
forms) make their appearance. The latter sometimes occur in 
great numbers in crops (blood-crises). The leukocytes are usually 
normal in number and kind ; but in some cases myelocytes have 
been met with. 

During the process of recovery from chlorosis the red corpus- 
cles increase in number before any change occurs in the percentage 
of hemoglobin. 

Pathologic Physiology. — Chlorosis resembles the second- 
ary anemias in most particulars, as far as its influence on the general 
health is concerned. Some of the symptoms (cardiac and men- 
strual) are doubtless due to primary abnormalities of structure. 
The preservation of the subcutaneous fat despite advancing anemia 
is a striking feature. It is explained by von Noorden by the 
assumption that the quiet and warmth which chlorotics find neces- 
sary to their comfort lead to accumulation of fat. Decreased 
oxidation is certainly not the cause. 

PROGRESSIVE PERNICIOUS ANEMIA. 

Definition. — Progressive pernicious anemia is a form ot 
extreme anemia tending to increase in severity to a fatal end. It 
may be apparently causeless, or more or less adequate causes may 
be discovered. It is characterized by excessive oligocythemia 
and marked changes in the red corpuscles. 

Etiology. — The disease was described by Addison as a wholly 
causeless anemia — that is, an anemia independent of precedent 
disease of any sort. In recent years, however, causes of various 
sorts have been discovered. Pernicious anemia may occur in 
childhood or old age, but is usually met with at or after middle 
age. Depressing emotions, fright, exposure, and unsanitary sur- 
roundings may act as contributing causes. Among the more 
definitely active influences are : pregnancy and lactation, gastro- 
intestinal diseases, and intestinal parasites. Pregnancy and lacta- 
tion are frequent causes, but their manner of operation is obscure. 
Gastro-intestinal diseases of various sorts have been found in cases 
of pernicious anemia, including atrophy of the gastric and duo- 
denal mucosa, ulcerations, carcinoma, etc. The manner of opera- 
tion of these is obscure, though recent experimental work, tending 
to show that pernicious anemia is hemolytic in nature, suggests 
that poisons are generated in the gastro-intestinal tract, and, gain- 
ing access to the blood, cause its destruction. Among the evi- 
dences favoring this hemolytic theory, beside that furnished by 
direct experimental intoxication, are the peculiar pigmentation of 



332 



TEXT-BOOK OF PATHOLOGY. 



the liver and the excess of coloring-matter in the urine. Of the 
intestinal parasites that occasion a pernicious form of anemia, the 
Anchylostoma duodenale and Bothriocephalic latus are important. 
Other parasites occasionally cause severe anemia, but rarely, if 
ever, forms suggesting true pernicious anemia. The manner of 
production of anemia by parasites is still obscure. Some have 
held that the loss of blood (especially in the case of Anchylostoma) 
is the important cause ; but there are instances in which but 
little blood is lost. Others believe that the parasites generate 
poisons in their life or by decomposition after their destruction, 
and that these poisons act as hemolytic agents. 

In addition to the above, hemorrhages, systemic diseases (ma- 
laria, syphilis, and tuberculosis), and various kinds of infection 
have been considered as causes. Among the infectious agents 
various bacteria and protozoan organisms have been described. 
None of these seems to be of importance. 

Pathologic Anatomy. — Various secondary changes are met 
with, those in the blood-making organs being most important. 
The bone-marrow of the long bones is red and softened and 
often quite hemorrhagic (for details, see Bone-marrow). This 
change was formerly regarded as a primary and causal one. At 
the present time it is looked upon as secondary and reactive to 
the severe anemia. It represents the effort of the bone-marrow to 
compensate for the active blood-destruction. The spleen is some- 
times enlarged, and may be considerably so. (Pigmentation of 
the spleen will be referred to below.) 

The liver, kidneys, and especially the heart suffer degenerative 
changes (fatty) in severe cases. Similar alterations in the blood- 
vessels may cause punctate hemorrhages (especially in the retina), 
or larger hemorrhages in various situations. The lesions of the 
gastro-intestinal tract have been referred to. Some of them are 
doubtless secondary to the anemia ; others may be primary. 

Degenerations of the posterior and lateral columns of the spinal 
cord are frequent. They seem to be due to a toxic agent rather 
than to hemorrhages. 

Pigmentation of the liver, spleen, kidneys, and other organs is 
a significant condition in evidence of the active hemolysis supposed 
to occur in this disease. The pigmentation of the liver is most 
important, and seems to be characteristic. It occurs in the hepatic 
cells of the periphery of the lobules and in the endothelial cells of 
the lymphatic channels and capillaries in the same situation. The 
pigment is iron-containing, and may be well demonstrated by ap- 
plying the iron reactions (sulphid of ammonium ; hydrochloric acid 
and ferrocyanid of potassium — forming Prussian blue). 

The Blood. — The color of the blood is often strikingly pale ; 
though it may be dark in spite of marked anemia. The specific 
gravity is reduced. The marked feature of the disease is pro- 



DISEASES OF THE BLOOD. 



333 



nounced oligocythemia. This progresses rapidly, and in ordinary 
cases the number of red corpuscles sinks to 1,000,000 or less per 
cu.mm. : at the same time changes in size (microcytes and megalo- 
cytes) and in shape (poikilocytes) make their appearance, and 
reach grades rarely attained in other diseases (see Fig. 145). Nu- 



Fig. 145. — Blood in pernicious anemia, showing irregularity in the size and shape of 
the red corpuscles; one nucleated red corpuscle (megaloblast) and two leukocytes ; stained 
with Ehrlich's triple mixture. 

cleated red corpuscles are always present in some number and 
are usually abundant (Fig. 145). The larger forms (megaloblasts), 
as a rule, predominate ; but in some cases the smaller forms are 
more abundant. Karyokinetic figures may be found in the nuclei. 
Polychromatophilia is generally present. The leukocytes may be 
decreased or normal in number ; in the late stages leukocytosis is 
not uncommon, and it may become extreme. The larger mono- 
nuclear leukocytes are usually more abundant than in health, and 
myelocytes often occur in considerable numbers. In the terminal 
leukocytosis of pernicious anemia the lymphocytes often predomi- 
nate. 

The fibrin-factors have been found in increased quantity in 
chemical examinations, and albumoses (peptone ?) and excessive 
quantities of xanthin-bodies have been detected in some cases. 

Pathologic Physiology. — Pernicious anemia has many 
characteristics of an intoxication, and there are undoubtedly toxic 
bodies in the blood, whether these be essential or incidental. Some 
investigators claim to have obtained putrescin and cadaverin from 
the urine. There is more active metabolic tissue-consumption than 
in health ; but the relations of oxidation to some of the secondary 
lesions of the disease require further study. 

Leukemia. 

Definition. — Leukemia is a disease of hemogenesis, character- 
ized by increase in the number of leukocytes in the circulating 



334 



TEXT-BOOK OF PATHOLOGY. 



blood and by pathologic changes in the bone-marrow, spleen, and 
lymphatic glands. 

©tiology. — Various diseases (malaria, syphilis, rickets, etc.) 
have been regarded as predisposing causes. The same is true of 
pregnancy, lactation, traumatism, exposure, and other influences. 
Sometimes heredity seems to be an important element. 

Infection has been suspected as the direct cause of leukemia by 
many observers, and various forms of bacteria have been discovered 
in the blood and tissues. There are certainly some very striking 
facts in favor of an infectious nature, the most important being the 
apparent contagiousness in a few cases. The various micro-organ- 
isms need not be enumerated, as none of them has been proved to 
be pathogenic. Bodies resembling protozoa have been found in 
the blood and in the organs (lymphatic glands), but the nature and 
significance of these are uncertain. 

The relations of the lymphatic lesions to the condition of the 
blood requires consideration. Virchow held that active prolifera- 
tive change in the lymphadenoid tissues is the pathologic foun- 
dation of the disease and the source of the increased numbers of 
leukocytes in the blood. This view was strongly supported by 
Flemming's discovery of karyokinetic changes in the cells of the 
lymphatic glands and spleen. Another school of pathologists 
maintained that the increased proportion of leukocytes results 
from retardation in leukocytic destruction, and that the peculiar 
lesions of the lymphadenoid tissues result from the deposit of the 
leukocytes from the blood. Most authorities agree that there is some 
deposition of this kind, but hold to the view of Virchow that the 
enlargement of the lymphatic organs comes in the main from 
primary disease of the affected parts. 

Pathologic Anatomy. — The lesions of the solid organs 
principally occur in the spleen, the bone-marrow, and the lymphatic 
glands, and the terms lienal or splenic, medullary or myelogenous, 
and lymphatic leukemia are applied. In the majority of cases the 
spleen and bone-marrow are involved, and the name lienomedul- 
lary leukemia is used. Pure lymphatic leukemia is comparatively 
rare, but involvement of the lymphatic glands with the spleen 
and bone-marrow is common. A few cases of pure myelogenous 
leukemia have been described, but their nature was not certainly 
determined. 

(The changes met with in the lymphatic structures are discussed 
in the appropriate sections and in the chapters on Tumors.) 

In a few instances the primary lesion was lymphadenoma of 
the thymus gland or its remnant. Occasionally the primary dis- 
ease is in the lymphadenoid tissues of the gastro-intestinal tract. 
Primary dermal leukemia has been described (lymphodermia 
perniciosa), but is not satisfactorily established. 

Among the secondary lesions are lymphoid infiltrations of the 



DISEASES OF THE BLOOD. 



335 



liver, kidneys, lungs, heart, and other tissues. The organs show 
areas of light color, or a streaked or mottled appearance, due to 
the deposition of masses of lymphoid cells (Fig. 146). Secondary 




Fig. 146.— Lymphoid infiltrations between the renal tubules, from a case of leukemia. 

degenerations of the heart, liver, and kidneys may result from the 
lymphomatous deposits, or from the impoverished state of the 
blood and the presence of toxic substances. Scleroses of the 
spinal cord may be met with, as in pernicious anemia. 

The Blood. — The blood is often light in color and may be quite 
milky in appearance. The specific gravity is lowered. The 
alkaline reaction is less decided than normal, and in some cases 
the reaction has been found acid, probably from rapid change after 
removal from the body. Coagulation is slow. This has been 
attributed to the presence of albumoses in the blood. 

The conspicuous feature in the blood is the increased number 
of leukocytes. In moderate cases there are from 100,000 to 300,- 

000 white corpuscles per cu.mm. In severe cases the number is 
greater ; while in mild or beginning cases, or in cases under active 
treatment, the number may for a time be normal or subnormal. 

1 have at the present time under observation a case in which the 
leukocytes have fallen to 3,000 from 500,000 per cu.mm. Rapid 
fluctuations in number are very common. 

The study of the blood led Virchow to distinguish two forms 
of leukemia : that in which small forms of leukocytes pre- 
dominate (lymphemia), and that marked by the excessive number 
of large cells (splenemia). This distinction may still be made, 
but the significance attributed to it as an indication of the organs 
primarily affected cannot now be sustained. It is true that in 
lienomedullary leukemia large cells usually predominate, while 
lymphocytes are conspicuous in lymphatic forms of leukemia ; but 



336 



TEXT-BOOK OF PATHOLOGY. 



transitional cases rob the distinction of its practical importance. 
It is here retained for the sake of convenience of description. 

Lienomedullary Type. — The blood presents a great excess of 
white corpuscles and more or less decided poverty in red cells. 
The proportion of white to red corpuscles is often 1 : 3, 1 : 2, or 
even 1:1. The larger mononuclear leukocytes (including normal 
mononuclear and transitional elements and myelocytes) predomi- 
nate over the lymphocytes and polymorphonuclear elements (Fig. 
147). The latter two forms, however, are actually increased. 




Fig. 147. — Blood in lienomedullary leukemia, showing several mononuclear neiitro- 
philes (myelocytes), one polymorphonuclear neutrophile, and an eosinophile ; a nucle- 
ated red corpuscle and a lymphocyte are seen in the lower part of the illustration ; stained 
with Ehrlich's triple mixture. 

Myelocytes are usually found in great numbers, and are an evi- 
dence of implication of the bone-marrow. There is usually an 
actual increase in the number of eosinophile elements, but the 
percentage-proportion is rarely increased. Basophilic leukocytes 
(mast-cells and finely basophilic forms) are present in numbers 
greatly in excess of those found in health. The red corpuscles 
present the usual features of anemic blood, and nucleated forms 
are particularly abundant. This is regarded as an evidence of 
disease of the bone-marrow. 

A peculiar constituent of the blood are the Charcot-Neumann 
crystals. These are polyhedral, needle-shaped crystals of un- 
certain composition, met with in the blood after death or some 
time after removal from the body, and exceptionally in the fresh 
blood. They were first detected in the bone-marrow. 

Lymphatic Type. — The leukocytosis is less marked than in the 
lienomedullary type. The lymphocytes predominate (Fig. 148), 
but actual excess of large mononuclear forms and polymorpho- 
nuclear leukocytes is observed. Myelocytes occur in small num- 
bers ; exceptionally in considerable proportion. The number of 
red corpuscles is decreased, and nucleated red cells may be present. 



DISEASES OF THE BLOOD. 



337 



Pathologic Physiology. — Leukemia is usually a progres- 
sively destructive disease. The nature of the disturbances, how- 
ever," is only partly known. The blood contains toxic substances 
generated by leukocytic destruction (xanthin-bodies) and acids 
(lactic, acetic, etc.). Albumoses are present in varying propor- 




Fig. 148.— Lymphatic leukemia, showing excess of lymphocytes. 

tions, and probably play an important part in the pathology. The 
urine frequently contains excess of xanthin-bases and uric acid. 

Acute I/etlkemia. — In a certain number of cases leukemia 
seems to run an acute course, terminating in from a few weeks to 
a few months. The characters of the blood are much the same as 
in ordinary chronic leukemia (especially the lymphatic type), and 
the lesions are similar. Gastro-mtestinal lesions (ulcers in the 
mouth, stomach, or intestines) and petechial hemorrhages (pur- 
pura) are frequent. In several instances distinct contagiousness 
was noted. The exact pathology of this condition remains obscure ; 
it is very probable that there is some form of acute infection. 

Hodgkin's Disease. 

Pseudoleukemia, or Hodgkin's disease, resembles leukemia in 
the lesions of the solid organs, but differs in that the blood does 
not present increase in the number of leukocytes. The lymphatic 
glands enlarge more quickly than in leukemia and the spleen and 
marrow are less frequently involved, but otherwise no distinction 
can be made. Cases of Hodgkin's disease sometimes become con- 
verted into leukemia, and the reverse has been known to take 
place. It has been held by some that Hodgkin's disease repre- 
sents an aleukemic stage of the same disease. 

Pseudoleukemia Infantum. 

Under this name von Jaksch described a form of leukocytosis, 
with enlargement of the spleen and liver, occurring in children. 

22 



338 



TEXT-BOOK OF PATHOLOGY. 



There is rapid and excessive oligocythemia, and the leukocytosis 
is pronounced. Leukocytes of all types are present, and give to 
the blood a curiously variegated appearance. There is no striking 
difference, however, from the characters of the blood met with in 
other cases of leukocytosis in infancy. Rickets and congenital 
syphilis seem to be closely related to this form of disease. 

The enlargement of the spleen and liver is not of the nature 
of that seen in leukemia or Hodgkin's disease, but is simply a 
chronic hyperplastic condition. 

FOREIGN BODIES AND PARASITES. 

Foreign Bodies in Blood. — Various kinds of particles may 
gain access to the blood-current and may be carried to peripheral 
parts of the circulation. In anthracosis a lymphatic gland may 
attach itself and, after softening, rupture into a vein. The parti- 
cles of carbon are thus distributed in the blood. Small portions 
of tumors, of the heart-valves, calcareous particles from atherom- 
atous plates, and portions of thrombi are frequently transported by 
the blood. Charcot crystals are met with in leukemia, and pig- 
ment-matter, due to disintegration of the blood itself, is seen in 
malaria. 

Parasites in the Blood. — Among the animal parasites are 
the malarial plasmodium, which occurs within the red corpuscles 
or free in the plasma ; the Distoma haematobium, which occupies 
the portal vein ; and the embryos of the Filaria sanguinis hominis. 
(These are more fully described in the section on Parasites.) Por- 
tions of hydatid cysts or of cysticerci and trichina? are occasionally 
conveyed in the circulation. 

Vegetable Parasites. — Mould-fungi sometimes gain entrance 
into the circulation and lead to serious embolism, as does also the 
streptothrix actinomyces. Of the pathogenic bacteria, the spiril- 
lum of relapsing fever and the bacillus of anthrax are most 
abundant in the blood. Other micro-organisms are more difficult 
of demonstration, though micrococci of suppuration, the bacillus 
of influenza, and even tubercle-bacilli have been detected. 

METHODS OF EXAMINING THE BLOOD. 

The purely clinical examinations, such as the enumeration of 
the corpuscles and the estimation of the percentage of hemoglobin, 
need not be here described. The microscopic examinations alone 
will be considered. 

Examination of the Fresh Blood. — A drop of blood is 
obtained from a prick into the end of a finger or the lobe of the 
. ear. The finger or ear is first cleansed, then pricked with a lancet, 
and the first few drops of blood wiped away. A small drop is 
then received upon a carefully cleansed thin cover-glass, and this 
is laid on an equally clean and slightly warm glass slide. The 



DISEASES OF THE BLOOD. 



339 



blood spreads into a thin film from the weight of the cover-glass. 
If prolonged examination is to be made, a ring of vaselin around 
the edges preserves the specimen for some hours. 

The examination should be made with an oil-immersion lens. 
Malarial parasites, the spirocheta of relapsing fever, and filarise 
are quite readily detected in such specimens ; sfnd the size and 
shape of the red corpuscles and the ameboid movements of the 
leukocytes can be determined. For the last purpose a warming- 
stage is requisite if a prolonged examination is to be made. 

Examination of Fixed Preparations. — Thin cover-glasses 
are carefully cleaned with soap-water, then with clear water, and 
finally with alcohol. A drop of blood is placed upon one of the 
glasses and a second glass is laid upon it. The blood spreads into 
a thin film, and the cover-glasses are then slid apart and allowed 
to dry in air. 

Fixation of the blood may be accomplished by immersing 
the prepared cover-glass in a mixture of equal parts of absolute 
alcohol and ether for from five to thirty minutes. For certain 
stains (notably the neutrophilic mixture) a better method of fixa- 
tion is the employment of heat. The most accurate method of 
heating is to place the cover-glass in an oven at 120° C. (248° F.) 
for an hour ; but I find that drawing the cover-glass rapidly through 
a Bunsen flame three times accomplishes the purpose almost as well. 
Special methods of fixation, as with bichlorid of mercury, picric 
or osmic acid, etc., are rarely necessary. 

Staining. — A useful stain to determine the morphology of the 
corpuscles is Gollasch's mixture : 



Eosin crystals . . 0.5 

Hematoxylin 2.0 

Glycerin . 

Distilled water 

Absolute alcohol da 100.0 

Glacial acetic acid 10.0 

Alum slight excess. 



The solution must be allowed to " ripen " by exposure for sev- 
eral weeks in a light place. The specimen is stained for two or 
three minutes, washed in water, and examined. The various 
pathologic conditions of the red corpuscles are brought out, and 
the morphology of the leukocytes is well shown. The oxyphilic 
granules stain sharply with the eosin. 

Similar results are obtained with the following mixture : 

Methylene-blue, saturated aqueous solution 40 

Eosin, £ per cent, solution in 75 per cent, alcohol 20 

Distilled water 40 

The specimen may be stained for from three to five minutes, 
but better results are obtained by placing the stain containing the 



340 



TEXT-BOOK OF PATHOLOGY. 



cover-glass preparation in an oven at 37° C. (98.6° F.) for an hour. 
The morphology and changes in the red corpuscles are clearly 
shown, and the oxyphilic and basophilic granules of the leukocytes 
are well stained — the former red, the latter blue. The basophilic 
granules of the leukocytes are especially distinct. 

Neutrophilic granules are best stained with Ehrlich's triple 
stain : 



Orange G, saturated aqueous solution 120 to 135 

Acid fuchsin, saturated aqueous solution 80 to 165 

Methyl-green, saturated aqueous solution 125 

Distilled water 300 

Absolute alcohol 200 

Glycerin 100 



The first two stains are mixed, and the third is added gradu- 
ally, stirring constantly. The water, alcohol, and glycerin are then 
added. Very often less acid fuchsin and more methyl-green give 
better results. The fixed preparation is stained for three minutes 
and washed in water. The red corpuscles take the orange stain ; 
the nuclei of white and red corpuscles and basophilic granules 
take the green ; the oxyphilic granules take the red ; and the 
neutrophilic granules take the violet or purple of the mixture. 

Staining of Parasites. — The malarial parasites may be 
satisfactorily examined in unstained specimens, but it is sometimes 
desirable to study them after staining. Cover-glass preparations 
are made as before described, and fixed by heat or by immersion 
in the absolute alcohol-ether mixture for from thirty minutes to 
several hours. The staining may be accomplished with any of the 
various eosin-methylene-blue mixtures, but Plehn's solution has 
been specially recommended for the purpose : 



Methylene-blue, saturated aqueous solution 60 c.c. 

Eosin, J per cent, solution in 75 per cent, alcohol 20 c.c. 

Distilled water 40 c.c. 

Potassium hydrate, 20 per cent, solution 12 gtt. 



This stains the malarial organisms blue, the red corpuscles red. 
Similar solutions stain filarial satisfactorily, and are useful in 
demonstrating various bacteria in the blood. 



CHAPTER II. 

DISEASES OF THE LYMPHATIC TISSUES. 

THE SPLEEN. 

Anatomic Considerations. — The spleen is practically a 
complicated lymphatic gland with close relations to the circula- 
tion. It is enclosed in a fibrous capsule, from which trabecular 



DISEASES OF THE LYMPHATIC TISSUES. 



341 



enter into the substance of the organ and give off subdivisions 
that unite and form a framework, in the meshes of which lym- 
phoid tissue is embedded. The splenic artery enters at the hilum 
and subdivides into numerous branches which traverse the tra- 
becule. Side branches are given off from the trabecular arterioles ; 
these penetrate the splenic pulp and are surrounded by denser- 
aggregations of lymph-cells, which are visible to the naked eye as 
the Malpighian bodies. All of the terminal arteries discharge 
their blood directly into the spaces of the splenic pulp, from which 
it is re-collected into the veins. The spaces contain, in addition 
to lymphoid cells and red blood-corpuscles, larger cells often con- 
taining pigment-granules or even small blood-corpuscles. 

The weight of the spleen in the adult varies from 140 to 
200 gm. 

The splenic function remains in doubt. It seems to have some 
connection with the process of manufacture of leukocytes, and is 
one of the sources of red blood-corpuscles. It may also be the 
place of destruction of red corpuscles, and in cases of general 
hemolysis, or blood-destruction, the blood-pigment and fragmented 
corpuscles are especially arrested in this organ. 

Pathologic Physiology. — The relations of diseases of the 
spleen to the general health are still obscure. It has been held 
by some pathologists that this organ plays an important part in 
the process of immunization or combating infectious diseases. The 
fact that bacteria and foreign bodies circulating in the blood are 
arrested in the spleen to such a large extent warrants the suspicion 
that this organ is important in arresting irritants, and thus pre- 
venting their gaining access to more vital parts. Experimenters, 
however, have found no uniform increase of susceptibility to micro- 
organismal inoculation on the part of desplenetized animals. For 
the present, therefore, we can only suspect that removal or disease 
of the spleen renders individuals more vulnerable to infections. 

The effect of removal of the spleen in human beings is sur- 
prisingly slight. A certain amount of anemia and general deteri- 
oration of health follow the operation, but seem to be the result 
of the operation per se, rather than of removal of the organ. Sub- 
sequently, complete health is regained. 

ABNORMAL DEVELOPMENT AND SITUATION. 

Complete absence of the spleen has sometimes been noted in 
children that lived for several years. More commonly slighter 
defects, such as unusual smallness or excessive lobulation, occur. 
Very often small accessory spleens, the size of a pea or a marble, 
are found. 

Movable Spleen. — The organ may be quite movable, either as 
a congenital condition or as the result of enlargement and resulting 



342 



TEXT-BOOK OF PATHOLOGY. 



traction upon its attachments. Downward displacement and 
movability are frequently found in cases of splanchnoptosis. 
Twisting of the pedicle of a movable spleen may lead to stran- 
gulation of the circulation and consequent necrosis. 

CIRCULATORY DISTURBANCES. 

Anemia may occur in cases of general anemia resulting from 
hemorrhage or inanition. The spleen presents a contracted appear- 
ance, the capsule being wrinkled, and on section the substance is 
found to be lighter in color and the fibrous stroma is more prom- 
inent than normal. 

Hyperemia may be active or passive. Active hyperemia is a 
physiologic condition during digestion, when the spleen increases 
somewhat in size. Intense congestion occurs in a number of dis- 
eases, but so commonly passes into inflammation that it will be 
described under that heading. Passive congestion is most marked 
in cases of cirrhosis of the liver, but also occurs in association 
with hyperemia of other organs as the result of cardiac failure, of 
emphysema, or of other diseases obstructing the larger venous 
channels. The spleen is greatly enlarged and of a dark-red color, 
and the capsule is often tensely distended ; the Malpighian bodies 
are less visible than normally. After long continuation of the 
process hyperplasia of the trabecular and the fibrous stroma gen- 
erally takes place. The spleen may be greatly enlarged and very 
dense at this stage. Subsequently contraction of the newly-formed 
fibrous tissue may lead to atrophy of the proper splenic substance 
and increased induration of the organ (cyanotic induration). Con- 
siderable pigmentation is found in such cases from the destruction 
of the stagnated blood. 

Hemorrhages in the spleen may be the result of traumatism, 
when large hematomata may form, especially just beneath the cap- 
sule. Small areas of hemorrhage are not infrequent in intense in- 
fections with splenitis, but it is difficult to draw a line between 
hemorrhage and the overfilling of the spaces by congestion, since 
the blood under normal conditions enters directly into the splenic 

Embolism of the splenic artery is very common in cases 
of endocarditis or thrombosis in the left heart or aorta. As the 
spleen contains abundant "terminal arteries/' infarction is the 
common result. The area may remain light colored, constituting 
an anemic infarct ; or it may become overfilled with blood, when 
hemorrhagic infarction results. In either case there is a wedge- 
shaped lesion, with the base toward the surface of the organ and 
the apex within, harder than the surrounding tissue, and usually 
somewhat elevated. The swelling and elevation in the case of 
anemic infarction are partly due to a zone of hyperemia which 



DISEASES OF THE LYMPHATIC TISSUES. 



343 



usually surrounds it. Complete resolution may occur, but more 
commonly the area involved undergoes coagulation-necrosis and 
softening, and as absorption takes place fibrous overgrowth gives 
rise to the formation of a scar. There may be numerous infarcts 
of small size, or a single large one sometimes occupying as much 
as half of the organ. (Septic infarction and its results are dis- 
cussed under Abscess of the Spleen.) 

Thrombosis of the splenic vein may occur in association with 
thrombosis of the portal vein. It causes intense passive hypere- 
mia of the spleen. Occasionally calcification of thrombi gives 
rise to the formation of splenic stones. 

INFLAMMATION OF THE SPLEEN, OR SPLENITIS. 

Splenitis occurs in a variety of conditions, and may present 
itself in several forms, among which the acute enlargement of the 
spleen of infectious diseases and localized splenitis, or abscess of 
the spleen, are the principal. 

Diffuse Splenitis. — The splenic enlargement of infection 
occurs particularly in typhoid fever, malaria, septicemia, typhus, 
and relapsing fevers; and less markedly in pneumonia, scarlet 
fever, small-pox, and influenza. In the earlier stage the spleen is 
simply congested and presents a dark-red color ; is firm, and the 
capsule more or less distended. On section the Malpighian bodies 
are usually obscured, and there may be visible areas of hemorrhagic 
extravasation. Microscopically at this stage the blood-vessels are 
all found overdistended, and the spaces within the splenic pulp are 
filled with red and white blood-corpuscles. If the process has con- 
tinued for some time, pigment-masses and degenerated corpuscles 
are visible, but there are as yet no evidences of inflammatory 
hyperplasia of the splenic pulp or stroma. 

As the process advances the spleen may become softer and may 
be quite diffluent. On section the substance is now found to be 
lighter in color, the Malpighian bodies are distinct, and, particu- 
larly in violent septic cases, are decidedly prominent, presenting 
themselves as yellowish-gray punctse, somewhat resembling miliary 
tubercles. The capsule of the organ may still be tensely distended, 
but in other cases is wrinkled, as if some shrinkage of the spleen 
had occurred in the change from the first stage of congestion to 
that of well-defined inflammation. Microscopically there is now 
apparent a great increase of the cells of the splenic pulp, particu- 
larly of those constituting the Malpighian bodies. That this in- 
crease is partly at least due to active proliferation is known from 
the abundance of mitoses. There is also hyperplasia of the stroma 
and trabecular, and of the endothelial cells of the spaces. 

In still later stages signs of degeneration may become promi- 
nent. This is apparent in the increasing softening of the organ, 



344 



TEXT-BOOK OF PATHOLOGY. 



while under the microscope there are found cellular degenerations 
leading to the formation of detritus, to fragmentation of the nuclei 
of the cells, and to pigmentation by disintegration of red blood- 
corpuscles. 

Terminations. — Most frequently complete resolution occurs. 
Sometimes, however, persistence of the inflammation is noted ; 
and, when repeated attacks of the infection occasion repeated 
attacks of splenitis, chronic inflammatory hyperplasia is the result. 
This is especially marked in the " ague-cake" spleen of malaria. 
Spontaneous rupture or rupture from slight trauma may result 
from the softened and distended condition of the organ. Finally, 
suppuration may ensue, either in the form of a diffuse softening 
and purulent infiltration of the entire organ, or in the form of a 
localized abscess beginning at the point of greatest involvement. 

Circumscribed Splenitis, or Abscess of the Spleen. — 
This may be the termination of an acute diffuse splenitis, particu- 
larly in septicemia and typhoid fever ; or it may be caused by 
extension of diseases of neighboring structures, by septic embo- 




Fig. 149— Embolic abscess of the spleen (from a specimen in the Museum of the Philadel- 
phia Hospital). 

lism, or traumatic injuries. In the last case, the mechanical 
injury of the spleen merely furnishes suitable conditions for the 
action of bacteria conveyed to it through the circulation, or the 
spleen is actually penetrated and infected. Occasionally abscess 
may result from the perforation of gastric ulcers or from the ex- 
tension of other inflammations in the vicinity. An important 



DISEASES OF THE LYMPHATIC TISSUES. 



345 



group of cases is that in which the abscesses are embolic and 
metastatic (Fig. 149). Such cases are met with in malignant 
endocarditis or thrombosis of the heart or aorta, and in cases of 
pyemia following other infective conditions. The first effect of 
the embolism is an hemorrhagic or anemic infarction, but this soon 
undergoes suppurative softening, beginning at the apex of the in- 
farct. Metastatic abscesses are most common near the surface of 
the organ and are usually multiple, though a single cavity occupy- 
ing the greater part of the organ may occur. Small collections 
may become absorbed or inspissated, leaving a necrotic or cheesy 
collection as a residue. Larger collections may be discharged by 
perforation into the stomach or intestines, or they may break into 
the peritoneal or pleural cavity, causing septic peritonitis or 
pleuritis. 

Chronic Inflammation or Chronic Hyperplasia of the 
Spleen. — Attention has already been called to the slow hyper- 
plasia of the connective tissue and sometimes of the splenic pulp 
occurring in consequence of chronic passive congestion and of re- 
peated attacks of acute splenitis. The spleen is large in size and 
firm. The capsule is often tensely distended and may be greatly 
thickened. The thickening is either diffuse or circumscribed, 
patches of almost cartilaginous hardness occurring in the latter 
case. Attachments by fibrous adhesions may fix the spleen to the 
diaphragm or the neighboring organs. On section the spleen is 
found dark in color from the presence of abundant pigment, and 
the excess of fibrous tissue may be visible to the naked eye. Mi- 
croscopically, increased thickness of the fibrous trabecular and of 
the walls of the small blood-vessels and pigmentation with altered 
blood-pigment are the conspicuous features. 

A somewhat different form of chronic hyperplasia is dependent 
upon syphilis, especially upon the congenital form. In this the 
appearances are much the same as in the cases following splenitis 
or congestion, but, as a rule, the color is somewhat lighter from 
the fact that the process is a slowly hyperplastic one without acute 
inflammatory or congestive manifestations. Somewhat similar 
appearances result from rickets. 

ATROPHY AND DEGENERATIONS. 

Atrophy of the spleen is very common in old age. The cap- 
sule is usually wrinkled and somewhat thickened, and on section 
the organ is more fibrous in appearance on account of atrophy of 
the splenic pulp and proliferation of the stroma. Thickening of 
the capsule sometimes appears in the form of white plates of 
cartilaginous hardness, which result from inflammatory over- 
growth of the capsule (perisplenitis cartilaginea). 

Amyloid degeneration occurs more frequently in the spleen 



346 



TEXT-BOOK OF PATHOLOGY. 



than in any other organ. The causes are those which lead to amyloid 
disease elsewhere. In most cases the degeneration begins in the 
Malpighian bodies, affecting the walls of the blood-vessels (Plate 
2) and the lymphoid elements. On section in such a case there 
are seen small round areas about the size of a currant-seed, of 
gelatinous, translucent appearance. These have been likened to 
grains of boiled sago, and the term sago-spleen is not inappropriate. 
In other cases a more uniform involvement of the whole organ is 
noted, and the section presents the appearance of boiled ham or 
dried beef. Considerable enlargement of the organ is noted in 
such instances, and the tissue is much harder than normal. 
Beginning amyloid degeneration may be difficult to determine 
microscopically, but is readily demonstrated by the microscopic 
staining-reactions (see Amyloid Degeneration). 

Hyaline degeneration has been observed in association 
with amyloid and independent of the latter. It affects the small 
blood-vessels and the reticulum more particularly. 

Pigmentation is a very common result of chronic congestion 
as well as of repeated acute splenitis ; the spleen in cases of 
cirrhosis of the liver and in chronic malaria is therefore habitually 
pigmented. The deposit occurs first in the walls of the blood- 
vessels and later throughout the splenic structure, either within the 
cells or lying free in the tissue. Occasionally pigment-particles 
derived from the external world are deposited in the spleen. This 
is especially true of dust-particles which have reached the circu- 
lation from softened bronchial glands. In cases of diseases of 
other kinds leading to discharge of foreign bodies or tissue-ele- 
ments into the circulation, the arrest not rarely occurs in the 
spleen, and reactive congestion or inflammation with enlargement 
of the spleen may result (spodogenous splenitis). Pigmentation of 
the spleen is seen in progressive pernicious anemia and other con- 
ditions in which hemolysis occurs. The pigments resulting from 
the destruction of red corpuscles are deposited in the liver, spleen,, 
and other organs. 

Calcification occurs in the thickened capsule of chronic 
splenitis and in old infarcts, tubercular or syphilitic areas, and 
occasionally in thrombi of the splenic vein. Parasitic cysts may 
be surrounded by calcification. 

TUMORS AND PARASITES. 

I/ymphadenoma of the spleen, as it occurs in the diseases 
leukemia and pseudoleukemia, like the alterations of the lym- 
phatic glands occurring in the same diseases, may properly be in- 
cluded among the tumors rather than among simple hyperplasia?. 
The disease is appropriately designated lymphadenoma or lympho- 
sarcoma. The spleen may perhaps be affected primarily in leu- 



Plate 2. 



fc*4 



% © % & r# 



4 f>9 » 



7 



Amyloid degeneration of the spleen, showing a degenerated Malpighian body 
specimen stained with hematoxylin and eosin. 



DISEASES OF THE LYMPHATIC TISSUES. 



347 



kemia (lienal or splenic leukemia), but is more likely always in- 
volved after the bone-marrow (spleno-myelogenous leukemia). 
The appearances of the organ in leukemia and in Hodgkin's 
disease are identical. In the earlier stages the spleen is 
enlarged and soft. On section there is evidence of intense con- 
gestion, while at the same time light-colored areas, representing 
enlarged Malpighian bodies, are visible throughout its structure. 
Subsequently the hyperplasia of the lymphoid structures increases 
and the organ becomes lighter-colored and harder than normal. 
The pressure exerted on the splenic pulp causes anemia, and 
granular or pigmentary degeneration of the cells, while anemic 
and hemorrhagic infarctions with subsequent necrosis are likely to 
form near the surface of the organ. The section of such a spleen 
presents a peculiarly variegated appearance, while the microscopic 
examination exhibits wide variations from the normal. The 
Malpighian bodies are found greatly enlarged, and are composed 
of aggregations of the ordinary lymphoid cells, together with 
larger round cells. Mitoses have frequently been demonstrated. 
The splenic pulp is degenerated, exhibiting large cells enclosing 
pigment-granules or red corpuscles and detritus. 

Sarcoma and Carcinoma. — Primary sarcoma of the round- 
celled, or flbro-sarcomatous, variety has been 
observed. Secondary sarcoma, particularly 
melanotic sarcoma, and secondary carcinoma 
are more common than primary growths. 

Cysts are occasionally discovered. They 
are small, and are probably due to dilatation 
of the lymphatic spaces or to atrophy and 
cystic degeneration of the Malpighian fol- 
licles. 

Fibroma, angioma, and lymphan- 
gioma are very rare. 

Parasites. — Pentastomum denticula- 
tum, ecliinococcus cysts, and cysticerci have 
been observed. 



INFECTIOUS DISEASES. 

Tuberculosis of the spleen may occur 
in the form of minute miliary tubercles, 
which have a grayish translucent appear- 
ance and are usually present in large num- 
bers, especially near the capsule. They may 
be distinguished from enlarged Malpighian 
bodies by their greater opacity and their grayish rather than yel- 
lowish color. Tuberculosis also occurs in the form of larger 
caseous nodules, especially in children (Fig. 150). In these cases 




Fig. 150.— Large caseous 
tubercles in the spleen of a 
child (Orth). 



348 



TEXT-BOOK OF PATHOLOGY. 



there are seen nodular masses the size of a pea or cherry studding 
the surface and deeper structure of the spleen. This form is called 
Affentuberculose by the Germans, from the resemblance of the large 
nodules to tubercles met with in monkeys. Histologic examination 
proves the nodules to be composed of aggregations of tubercles 
undergoing caseation. 

Primary tuberculosis of the spleen has never been observed. 

Syphilis may present itself in the form of syphilitic gummata, 
which are usually multiple and may be either small or large. They 
are distinguished by their central degeneration or by the fibrous- 
tissue striations at the exterior. 

Diffuse hyperplasia of the spleen is a frequent or almost con- 
stant lesion of congenital syphilis. 

THE LYMPHATIC GLANDS. 

Anatomic Considerations. — The lymphatic glands con- 
sist of accumulations of lymphadenoid tissue surrounded by a 
connective-tissue capsule. There may be distinguished an outer 
cortical and an inner medullary portion, the former consisting of 
spherical masses or follicles of lymphoid cells enclosed in a con- 
nective-tissue reticulum springing from the trabecule, the latter 
being composed of medullary cords similar to the former in struct- 
ure, but of elongated form. The afferent lymphatics enter the 
glands at the hilum and discharge the lymph into the cortical 
spheres ; the liquid filters slowly toward the medullary cords, 
where it eventually enters the efferent lymphatics. The medullary 
cords are surrounded by spaces lined with endothelial cells, the 
lymph-spaces. 

ATROPHY. 

Atr6phy of the lymph-glands occurs in old age and in various 
marasmic conditions. The glands suffer considerable diminution 
in size, the cellular elements being particularly affected ; they are 
therefore hard, dry, and often irregular in shape. Fatty infiltra- 
tion may occur simultaneously with atrophy, the gland in such 
cases preserving its size and having a decidedly fatty appearance. 

HYPERTROPHY. 

This is so closely allied to the conditions designated by the 
name of lymphadenoma that it is difficult to separate the cases 
which might be considered as strictly hypertrophy. 

DEGENERATIONS. 

Fatty infiltration is sometimes seen in cases of general 
obesity and also, as before mentioned, in atrophy of the glands. 
Amyloid degeneration is met with in cases of general amyl- 



DISEASES OF THE LYMPHATIC TISSUES. 



349 



oid disease, and particularly in the cases in which the intestines 
are affected. The lymphatic glands may, however, be independ- 
ently involved in cases of tuberculosis attended with suppuration. 
In such instances the adjacent lymphatic glands are most likely to 
suffer amyloid change. The morbid process rarely leads to marked 
alteration of the glands, but the amyloid material may be demon- 
strated by the staining-reactions peculiar to it. The connective 
tissue of the trabecule and around the blood-vessels is first 
affected ; later, the endothelial cells. 

Hyaline degeneration has been described. It affects the 
blood-vessels and connective tissue of the glands. 

Calcification not infrequently forms the terminal condition 
in cases of necrosis or induration of the glands in consequence of 
tuberculous or simple inflammation. There may be small calca- 
reous granules scattered through the gland, or the entire gland 
may be infiltrated. 

Necrosis may occur in consequence of tuberculous or syphilitic 
affections, or of simple inflammation. In the former cases, particu- 
larly in tuberculosis, the center of the gland or the entire gland 
becomes cheesy and soft, often liquefying and discharging the 
contents by rupture of the capsule. In consequence of simple 
inflammation, as in certain infectious fevers (typhoid, diphtheria, 
scarlet fever), a different form of necrosis is met with, areas of the 
gland becoming soft, pultaceous, and sometimes putrid. The 
gland may rupture, discharging its contents, or absorption of the 
liquid with inspissation and a pseudocaseous form of degeneration 
may result. Finally, the degenerated area may become calcareous. 

Pigmentation may follow acute inflammations or traumatic 




Fig. 151.— Anthracosis of a bronchial lymph-gland (Orth). 

injury of the glands, the extravasations of blood occurring in such 
conditions leading to hematogenous pigmentation. The blood- 
pigment occurs in granular masses within the cells of the stroma 
or Avithin the lymphatic cells themselves. Blood-pigmentation 



350 



TEXT-BOOK OF PATHOLOGY. 



may also occur in the glands adjacent to areas of hemorrhagic 
extravasation, the pigment in such cases reaching the glands 
through the lymphatic vessels and being deposited in the lymph- 
sinuses, or even in the follicles and cords. Analogous pigmen- 
tation from external sources may result from tattooing, and occurs 
regularly in the bronchial glands as the result of the inhalation of 
various dust-particles which penetrate the walls of the bronchioles 
and alveoli and eventually find their way to the bronchial glands 
through the lymphatic stream (anthracosis) (Fig. 151). The 
glands may be completely black in such cases, and the lymphatic 
circulation through them may be obliterated. Secondary inflam- 
matory changes result in most cases (see page 351). 

INFLAMMATION ; LYMPHADENITIS. 

Acute lymphadenitis is commonly secondary to inflamma- 
tions in the neighborhood, the irritants being carried by the 
afferent lymphatics. Sometimes direct extension of inflammation 
by contiguity of structure may lead to involvement of the 
lymphatic glands. Occasionally lymphadenitis is seemingly pri- 
mary in cases in which the infective irritants have caused no 
lesion at the portal of entrance to the body. 

Pathologic Anatomy. — The glands become enlarged, hyperemic, 
and considerably infiltrated with liquid. When the inflammation is 
intense there may be minute hemorrhages. Microscopically the 
lymph-sinuses are found distended with cells — leukocytes, red 
blood-cells, and proliferated and desquamated endothelial cells 
from the lining membrane of the sinuses. The follicles and cords 
are increased in size from infiltration and probably also from pro- 
liferation of the lymphoid cells. The process may become arrested 
and resolution to the normal condition may ensue. If mild inflam- 
mation of this character has continued for a great length of time, 
or if the condition is repeated, hyperplasia of the trabecular con- 
nective tissue, of the blood-vessels, and of the capsule of the gland 
may lead to a termination in chronic enlargement and induration 
of the glands. 

In cases of greater intensity of the infective cause, necrotic or 
suppurative changes may occur. In the cases of necrosis such as 
occur in typhoid fever and in diphtheria there may be noted small 
spots of yellowish-white color in the hyperemic glands, and subse- 
quently these undergo well-marked necrosis. Complete necrotic 
softening and even rupture of the gland may ensue, or, if the 
necrosis remains limited in extent, inspissation and sometimes 
calcification may terminate the process. 

Suppurative lymphadenitis is not uncommon. It is seen 
in the glands below Poupart's ligament in cases of infective wounds 
of the leg ; in the inguinal glands as a result of chancroid or gon- 



DISEASES OF THE LYMPHATIC TISSUES. 



351 



orrheal urethritis ; in the glands of the neck in association with 
diphtheritic, scarlatinal, or other inflammations of the throat, or 
following erysipelas ; in the axillary glands as a result of wounds 
of the arm ; and in the internal lymphatics in various infective dis- 
eases. The term bubo is applied to suppurative lymphadenitis of 
superficial glands. Of particular interest is the tendency to this 
condition in the plague of the East, or the bubonic plague (g. v.). 

Pathologic Anatomy.— The changes noted in the gland at the 
outset are similar to those in the simple inflammations, but under 
the microscope a greater accumulation of leukocytes is apparent, 
and the gland tends to soften, with the formation of more or less 
creamy pus. The capsule may prove resistant for a time, and 
reactive inflammation around may establish an additional wall. 
A single gland of a group may be affected, but more commonly 
the several glands are together involved. Eventually rupture 
may take place, but in instances in which the process has been 
circumscribed, inspissation of the pus and finally calcification may 
occur. 

In the most intense forms of lymphadenitis hemorrhagic or 
gangrenous conditions are developed. 

Chronic Iyymphadenitis leads to induration with enlarge- 
ment. It occurs as the result of repeated acute attacks or in con- 
sequence of long-continued irritation by particles carried to the 
lymphatic glands from some focus of disease. 

Pathologic Anatomy. — As a rule, the process affects the con- 
nective-tissue elements of the gland in particular, and there 
results a considerable amount of induration, sometimes associated 
with atrophy or necrosis of the proper lymphoid structure. Occa- 
sionally, however, the lymphoid elements themselves are hyper- 
plastic, and the normal relation of fibrous tissue, follicles, and 
medullary cords is preserved. 

Microscopically the overgrowth of the connective tissue spring- 
ing from the trabecular, from the blood-vessels, and from the 
reticulum of the lymphoid portions, is apparent. This may consist 
of round cells and fibrous connective tissue, or there may be a 
tendency to the formation of epithelioid cells and even giant-cells. 

Pathologic Physiology. — Inflammations of the lymphatic 
glands are the result of the arrest of irritants of various sorts 
carried to the glands in the lymphatic channels. This arrest not 
unlikely serves the purpose of a protection against general dis- 
semination of irritants, and may be of great importance in this 
way. Complete occlusion of the lymph-sinuses by deposition of 
solid particles (as coal-dust), or by disease of the glands, may 
obstruct the lymphatic flow entirely, and a retrograde inflammatory 
process may result from the damming back of infected lymph or 
from extension of disease along the lymphatic channels. 



352 TEXT-BOOK OF PATHOLOGY. 

INFECTIOUS DISEASES. 

Tuberculosis of the lymphatic glands is due in nearly all 
cases to infection by bacilli reaching the gland through the affer- 
ent lymphatics, though occasionally it would seem that hemato- 
genous infection occurs. Under the heading tuberculosis we must 
include what the older writers designated as scrofulous glands, for 
in the majority of such cases, if not in all, the disease is essentially 
tuberculosis, though the mode of infection is not always apparent. 

Morbid Anatomy. — The first visible change is the formation of 
small grayish nodules in the gland, and sometimes the eruption of 
these is attended with hyperemia and inflammation. Later, these 
tubercles increase in size and undergo caseous 
changes (Fig. 152) as elsewhere, and eventu- 
ally the entire gland may be converted into 
a cheesy mass, which may liquefy and not rare- 
ly discharges through the ruptured capsule. 
Microscopically, the first appearance is that of 
gray tubercles containing giant-cells and 
epithelioid cells, surrounded by a zone of 
round cells (Fig. 153). Later, the character- 
FlG * ^lknd^orth). 17131 ^" istic appearances of hyaline transformation 
and of caseation are observed. Sometimes 
the glands in tuberculosis become enlarged and harder than normal, 
and present areas of grayish color, but do not tend so markedly to 




Fig. 153.— Tuberculous lymphatic gland : o, recent tubercle with giant-cell (c) ; a lt inferior 
caseous tubercle with giant-cell (cj ; b, lymphadenoid tissue ; d, epithelioid cell (Ziegler). 

undergo necrosis. In these instances the microscopic examination 
presents foci composed for the most part of epithelioid cells, and 




DISEASES OE THE LYMPHATIC TISSUES. 



353 



much less abundant in round cells than are tuberculous tissues as 
a rule (Fig. 154). 




Fig. 154.— Tuberculous lymphatic gland : a, lymphadenoid tissue ; b, large round cells 
(epithelioid) ; e, large spindle-cells (Ziegler). 

Scrofula. — The tuberculous nature of scrofulous lymphadenitis 
was first shown by demonstrations of the infectiousness of the 




Fig. 155.— Tuberculous lymphadenitis of the cervical glands (from a case in the Children's 
23 Hospital). 



354 



TEXT-BOOK OF PATHOLOGY. 



softened glandular material when injected into animals. The 
micro-organisms themselves may be demonstrable in the earlier 
stages in the epithelioid or giant-cells, or lying between these ; 
but when the process is at all advanced it is extremely difficult or 
impossible to demonstrate bacilli. 

Individual Groups of Glands. — Among the more commonly 
affected groups of glands are the cervical (Fig. 155), the bronchial, 
and the mesenteric. Tuberculous cervical glands occasion consider- 
able tumors in the neck, and it is these in particular that have 
been classified as scrofulous. Not rarely they advance to complete 
softening, and rupture on the surface. Sometimes, however, they 
penetrate deeply, and may rupture into the trachea or esophagus, 
or into the pleural cavity. The mode of infection is rarely 
apparent, but in many cases no doubt the micro-organisms enter 
through the mucosa of the mouth or pharynx, or the tonsils, where 
they may or may not first occasion specific lesions. 

The bronchial glands are affected very frequently in cases in 
which the bacilli, entering through the lungs, have left no trace of 
tuberculous disease at the portal of entrance ; while in cases of 
actual tuberculosis of the lungs the bronchial glands are quite 
constantly involved (Fig. 156). The glands are usually cheesy and 




Fig. 156.— Tuberculous lymphatic glands at the bifurcation of the trachea (from a speci- 
men in the Museum of the Philadelphia Hospital). 

may become calcareous, but softening not rarely occurs. Perfora- 
tion of one of the bronchi may lead to acute bronchogenetic tuber- 



DISEASES OF THE LYMPHATIC TISSUES. 



355 



culosis of the lungs ; or the softened gland may diseharge into a 
large vein and thus oceasion miliary tuberculosis. 

The mesenteric glands are especially involved in children, this 
condition being known as tabes mesenterica. The infection occurs 
through the intestinal tract ; and has sometimes been found due 
to the ingestion of infected milk or meat. The intestines may 
first suffer, or the bacilli may penetrate the intestinal mucosa with- 
out causing local lesions. 

Syphilis. — Enlargement of the lymphatic glands may occur in 
the vicinity of the initial lesion during the primary period ; and 
is habitually present in all parts of the body during the second- 
ary period, the post-cervical, axillary, inguinal, and epitrochlear 
groups being most characteristically involved. The glands are 
hard, and do not tend to soften or suppurate. Microscopically 
there is found proliferation of the connective-tissue elements 
throughout the gland. 

In the tertiary period gummata (bubo tertians) may be ob- 
served, especially in the lymphatic glands adjacent to the diseased 
viscera. 

I/eprosy, actinomycosis, and other infections occasion- 
ally involve the lymphatic glands (see General Pathology). 

TUMORS. 

I/ymphadenonia ; lymphosarcoma. — The term lymph- 
adenoma has been applied to certain enlargements of the lymphatic 
glands in which the appearance and structure resemble closely 
those of the normal gland. The nature of many of such cases is 
obscure, and very likely widely varying diseases have been in- 
cluded. In some instances repeated irritation has occasioned a 
functional hypertrophy or chronic inflammation of the gland, 
while in others, doubtless, infectious diseases (especially tuberculo- 
sis) may have been mistaken for tumors. We may restrict the 
term lymphadenoma to apparently causeless enlargements of the 
lymphatic glands in groups. In some cases the disease tends to 
involve the glands in all parts of the body, as well as to invade 
the spleen, the liver, the kidneys, and other organs. Enlarge- 
ments of this sort occur in leukemia and Hodgkin's disease (Fig. 
157). In cases of localized enlargements of the lymphatic glands 
it is likely that local irritation, as a rule, plays a prominent part 
in causation. 

Pathologic Anatomy. — Two forms of lymphadenoma have been 
described, the hard and the soft. In the former the glands of the 
group are enlarged and hard, the capsule is thickened, and ' the 
trabecular increased. Microscopically there is evidence of exces- 
sive proliferation of connective tissue, though overproduction of 
lymphoid elements may occur at the same time. In soft lymph- 



356 



TEXT-BOOK OF PATHOLOGY. 



adenoma the gland has much of its natural appearance, although 
it is somewhat more opaque and grayish. There is no tendency 
to soften or suppurate, and the individual glands of a group, 
though closely held together, do not fuse entirely. The distinction 
of lymph-sinuses, follicles, and medullary cords is less marked than 
normally, and the appearance is that of a uniform lymphoid 




Fig. 157.— Hodgkin's disease, showing marked enlargement of the glands of the right 
axilla, with consequent dropsy of the arm ; less marked involvement of the submaxillary, 
cervical, and inguinal lymph-glands. 

tissue composed of a cellular reticulum in which small round cells 
are embedded. From an anatomical standpoint the term lympho- 
sarcoma is applicable, and still more from the fact that nodular 
infiltrations with enlargement are usually found in the spleen as 
well as in organs which do not normally contain lymphatic tissue, 
such as the liver, the kidneys, and the heart. In some cases of 
lymphosarcoma the blood contains excess of leukocytes. These 
cases are known as leukemia. In other cases, though anatomical 
differences are not detectable, the blood contains no excess of 
leukocytes. These cases may present the clinical features of a 



DISEASES OF THE LYMPHATIC TISSUES. 



357 



progressive anemia, and are known as Hodgkin's disease, or 
pseudoleukemia. In occasional instances transformation of Hodg- 
kin's disease into leukemia, or the reverse, takes place, and there 
seems to be no well-established dividing-line between the two 
conditions (see, also, Lymphadenoma, in Part I.). 

Sarcoma. — Other forms of sarcoma are sometimes met with 
as primary localized new growths of the lymphatic glands. Such 
are not rarely seen in the mediastinum. In these instances the 
capsule of the gland is penetrated and local extension to neigh- 
boring glands and other surrounding structures is commonly 
observed, but the entire group of glands is not, as a rule, affected. 
General metastasis may occur, but affects the larger organs rather 
than the lymphoid tissues. Round-cell, spindle-cell, alveolar 
sarcoma, and endothelioma are the forms described. Secondary 
sarcoma occasionally involves the lymphatic glands. 

Carcinoma is always secondary, the lymphatic glands being 
the most frequent seat of secondary cancer. 



BONE-MARROW. 

Anatomic Considerations. — The marrow of the bones is 
a lymphadenoid tissue consisting of a reticulum of connective- 
tissue cells, supporting a rich network of capillaries and venules 
of unusual width. The cells proper of the marrow are rounded 
and vary greatly in size. They contain a clear nucleus, and many 
of them neutrophilic granules. In addition to these marrow-cells 
there are occasional giant-cells lying near the bony trabecular ; and 
more frequently cells containing pigment-granules ; also nucleated 
red corpuscles, non-nucleated red corpuscles, and large cells en- 
closing corpuscles. After the first few years of life the marrow 
of the long bones loses its reddish color and becomes more or less 
yellow, and there is then found, microscopically, a great pre- 
ponderance of fat-cells. 

DEGENERATIONS. 

Fatty Infiltration. — The fat which occurs normally in the 
marrow may be excessively developed in conditions of general 
obesity, but also at times in marantic individuals, or as a result of 
atrophy of the bony tissues. 

Mucoid degeneration is occasionally seen, and necrosis 
may form a part of the processes of inflammation. 

Pigmentation occurs in the bone-marrow in cases of destruc- 
tion of blood, as in malaria or various hemolytic toxemias, as the 
bone-marrow is one of the filtering organs for the blood. 



358 



TEXT-BOOK OF PATHOLOGY. 



ATROPHY. 

Atrophy of the bone-marrow is not infrequent in old age or in 
marasmic conditions. 

HYPERTROPHY. 

Hypertrophy of the bone-marrow occurs in various anemic 
diseases. Strictly speaking, there is atrophy or disappearance of 
the fat-cells of the yellow marrow of the long bones and hyper- 
plasia of the true lymphoid elements. The bone-marrow, there- 
fore, assumes more and more the appearance of the red or lym- 
phoid marrow of early life. The highest grades of this transfor- 
mation are met with in progressive pernicious anemia (Plate 3, 
Fig. 1) and in leukemia, but similar changes occur in cancer, tuber- 
culosis, and various other cachectic conditions. The marrow be- 
comes soft and red in color, and in extreme cases may be dark- 
red and liquid. 

Microscopically the fat-cells are much reduced in number and 
may be wholly wanting. In their place are found marrow-cells 
of various sizes, many of them containing neutrophilic and eosino- 
philic granulations. Cells containing pigment-granules or red 
blood-corpuscles, and nucleated red blood-corpuscles of different 
sizes, are seen in varying numbers. 

In leukemia the marrow often has a mottled appearance, light- 
colored areas composed largely of white corpuscles arrested in the 
marrow or formed in loco by active proliferation, alternating with 
darker areas of congestion or hemorrhagic extravasation (Plate 3, 
Fig. 2). The light-colored areas may predominate and may pre- 
sent a puriform appearance (pyoid marrow). More rarely the ap- 
pearance of the marrow in leukemia is similar to that seen in the 
other anemic diseases. Microscopically a curious constituent i& 
discovered — the Charcot- Neumann crystals (see Leukemia). It 
has been held that leukemia is dependent primarily upon the dis- 
ease of the bone-marrow (myelogenous leukemia), but the marrow- 
changes, in some cases at least, are secondary. 

INFLAMMATION. 

Osteomyelitis, or inflammation of the marrow, is infectious 
in nature, and may occur in the course of various diseases, such as 
typhoid fever, relapsing fever, small-pox, septicemia, and the like ; 
or as a result of traumatism and direct infection. The marrow- 
disease may be the only expression of an infection which has 
arisen in an obscure manner (infectious osteomyelitis). In the 
cases occurring in the course of infectious diseases, the changes are 
comparable to those which occur in the spleen under the same cir- 
cumstances. The marrow assumes a redder color than normal, 
and it may be studded with punctate hemorrhages. In other 



Plate 3. 




DISEASES OF THE LYMPHATIC TISSUES. 



359 



cases areas of necrosis and granular degeneration of the cells may 
be present, and increased numbers of lymphoid cells or white 
blood-corpuscles may be discovered. Sometimes the marrow is 
quite purulent (see Diseases of Bone). 

INFECTIOUS DISEASES AND TUMORS. 

(These will be referred to in the discussion of Diseases of the 
Bones.) 

THE THYMUS GLAND. 

Anatomy and Development. — The thymus gland at its 
earliest period consists of endodermic epithelium arranged some- 
what like that of an epithelial gland. Later, mesoblastic lymphoid 
cells and connective tissue infiltrate it ; and at birth and for several 
years thereafter it is composed largely of lymphoid tissue arranged 
like the follicles of lymphatic glands. Here and there in the cen- 
ter of these may be seen concentric whorls (the corpuscles of 
Hassall), the remains of the original epithelial cells. After the 
second year of life retrogressive changes take place, and by the 
age of adolescence the gland is converted into a mass of fatty con- 
nective tissue. 

Congenital Abnormalities. — Complete absence or various 
minor irregularities of the thymus may occur ; at times it is found 
enormously hypertrophied. In the latter case the root of the 
great vessels, the pericardium, and heart may be covered over by 
the enlarged thymus, and sudden death seems at times due to this 
cause. Thymic asthma, so-called, is rarely, if ever, due to enlarge- 
ment of the thymus. 

Circulatory Disturbances. — Intense congestion and punc- 
tate hemorrhages may be found in cases in which death has occurred 
from asphyxia. 

Inflammation of the thymus as a primary disease is of doubt- 
ful occurrence, but abscesses may occur in cases of general pyemia, 
or from extension of suppurative affections of adjacent parts. 

Infectious Diseases. — Syphilis occurs in the form of gum- 
mata, especially in the new-born. Caseation and softening of the 
gumma may occur, and a resemblance to abscess is thus produced. 
Miliary or caseous tuberculosis occasionally invades the thymus gland. 

Tumors. — The thymus or its remnant is not infrequently the 
place of origin of lymphosarcoma of the anterior mediastinum 
(see Fig. 47). Tumors having this origin may be recognized by 
their shape and by the regularity of their outlines, the lympho- 
sarcomata (lymphadenomata) of the lymphatic glands of the 
anterior mediastinum having a more irregular lobulated appear- 
ance. Ordinary round-celled sarcoma has been described, and 
epithelioma springing from the corpuscles of Hassall has been 
seen in a few cases. 



360 



TEXT-BOOK OF PATHOLOGY. 



CHAPTER III. 
DISEASES OF THE CIRCULATORY SYSTEM. 

THE HEART. 

Development of the Heart. — At the earliest period of fetal life the 
heart is represented by a hollow tube, lying toward the ventral aspect of 
the neck. Later this assumes an S-shape, and still later a transverse con- 
striction marks the position which the auriculoventricular grooves subse- 
quently occupy. Finally, vertical grooves divide the lateral halves into 
the respective auricles and ventricles ; and the truncus arteriosus, which is 
at one of the ends of the primitive tube, becomes divided into two parts, 
forming the pulmonary artery and aorta. The separation of the cavities 
within is accomplished by the outgrowth of septa springing from the walls 
of the primary cavities. The septum dividing the ventricles is the first to 
appear, and springs forward from the posterior wall. Next a budding is 
seen in the position which is later occupied by the tissue between the 
auriculoventricular orifices of the two sides ; still later the auricular cavity 
is divided into two parts by a process beginning at the lower and posterior 
part. The septum which divides the truncus arteriosus is essentially con- 
nected with or is a part of the septum which separates the ventricles. All 
of these changes begin from the seventh to the ninth or tenth week of 
fetal life. 

Anatomic Considerations. — The heart consists of three 
layers, the endocardium, muscular layer, and pericardium. The 
endocardium is the inner lining of the organ, and is composed 
of a layer of endothelial cells resting upon a stratum of connective 
tissue.* It is continuous with the lining membrane of the arteries, 
and by duplications forms the valves. The muscle of the heart is 
arranged in lamella?. The fibers of the heart-muscle are peculiar 
in being branched and in being devoid of a sarcolemma. The 
pericardium resembles the endocardium in structure. 

The blood-vessels supplying the heart-muscle are branches of 
the coronary arteries. They divide and subdivide, and afford 
abundance of blood proportionate to the needs of so active an 
organ. The lymphatic system is equally developed. The ner- 
vous system includes numerous ganglionic centers in the furrows 
between the ventricles and between the auricles and ventricles. 
Other ganglion-cells are found within the muscle itself. 

Details regarding the gross structure of the organ need not be 
mentioned here. The weight of the heart in the adult male is 
about 300 g., in the adult female about 250 g. The volume of 
the entire organ in the adult male is about 290 to 310 cu.cm., in 
the adult female about 260 to 280 cu.cm. 

CONGENITAL DISEASES AND DEFORMITIES. 

Abnormalities of the heart may be discovered in the new-born, 
and are the result of developmental defects, or less commonly of 



DISEASES OF THE CIRCULATORY SYSTEM. 



361 



fetal endocarditis and myocarditis. The older pathologists at- 
tributed to inflammatory changes many of the conditions which 
more accurate knowledge of the development of the heart clearly 
indicates are the result of defects in development. 

Abnormality of Position. — The heart may retain its posi- 
tion high up toward the cervical region, and may even be entirely 
in the neck. Occasionally it is completely exposed, or, merely 
covered with pericardium, lies immediately beneath the skin, 
the sternum in such cases being divided in the middle line. 
Sometimes it lies beneath the skin of the abdomen. 

Abnormality in Si^e. — Congenital smallness, or hypoplasia, 
of the heart and aorta is occasionally observed. Particular atten- 
tion has been called to this condition in cases of chlorosis (see p. 383). 

Defective Development. — There may be complete absence 
of the heart in acardiac monsters. Sometimes the septa dividing 
the auricles and ventricles are wholly wanting and a bilocular 
heart results ; or the auricular septum alone is absent, when the 
organ is triloeular. More commonly than these conditions, the 
organ is completely reversed, lying on the right side of the body 
and having the blood-vessels entering it and leaving it reversed, 
so that the general venous blood enters the left auricle, the pul- 
monary blood the right auricle, while the aorta springs from the 
right ventricle and the pulmonary artery from the left. The 
abdominal viscera may be reversed at the same time, the liver 
being on the left, and the spleen on the right, side. This condi- 
tion is spoken of as dextrocardia. Other abnormalities in the 
arrangement and origin of the great blood-vessels, such as an 
undivided truncus arteriosus, are rare. 

Stenosis and atresia of the pulmonary artery result from abnor- 
mal situation of the septum which divides the truncus. Com- 
plete atresia is very rare. Stenosis is one of the commonest 
developmental defects of the heart, and in some cases is due to 
fetal myocarditis about the orifice. It may involve the root, the 
conus, or the trunk of the vessel. The septum of the ventricles 
is usually defective and the foramen ovale remains patulous. 
When the stenosis is considerable the pulmonary circulation is 
maintained by the persistence of the ductus arteriosus Botalli ; and 
the right ventricle is greatly hypertrophied. 

Stenosis and atresia of the aorta are less frequent than the same 
conditions affecting the pulmonary artery. They arise from the 
same cause, and are usually accompanied by the same defects of 
the septa and patency of the ductus arteriosus. Stenosis of the 
trunk of the aorta at the isthmus — i. e., at a point between the left 
subclavian artery and the mouth of the ductus arteriosus — is not 
infrequent in moderate degree. More rarely there may be almost 
complete atresia, or the aorta may be entirely wanting at this 
point. The circulation is maintained by collateral anastomosis 



362 



TEXT-BOOK OF PATHOLOGY. 



of the branches of the subclavian with the descending aorta. 
In all of these cases hypertrophy of the left ventricle is usually 
present. 

Defects of the ventricular septum may be unaccompanied by other 
abnormalities ; but, as a rule, they are of secondary importance, 
occurring in cases of abnormality of the pulmonary artery or aorta. 
The septum may be completely wanting, or there may be partial 
defects, these latter usually lying anteriorly and above, in what is 
known as the membranous portion, or the undefended space. 
Very frequently a patulous condition of the foramen ovale is 
present. 

Defects of the auricular septum are comparatively rare, but a 
patulous condition of the foramen ovale is one of the most frequent 
of congenital affections of the heart. It is due to the failure of 
the valve of the foramen to unite at the edges, as normally occurs 
some time after birth. Slit-like openings are seen very frequently 
in post-mortem examinations, while more decided patency is occa- 
sionally observed without other cardiac abnormalities. This is 
especially likely to occur when congenital atelectasis or some other 
pulmonary affection causes continuance of high blood-pressure in 
the right heart after birth. 

Stenosis and atresia of the auriculoventricular orifices are rare 
congenital conditions ; and in the former fetal endocarditis doubt- 
less plays an important part. When there is complete atresia the 
auricular septum must remain widely open and the septum of the 
ventricle is usually deficient and the ductus Botalli patulous. 

Patulous Ductus Botalli. — This condition is frequent in cases of 
stenosis of either the aorta or pulmonary artery, and serves to con- 
vey the blood from the patulous artery into that which is obstructed. 
Like the patulous foramen ovale, it may occur as an independent 
condition resulting from congenital atelectasis of the lung which 
leads to the continuance of the fetal conditions of circulation. 

Valvular Defects. — Not rarely there may be but two semilunar 
valves at the aorta or pulmonary orifice, and, on the other hand, 
four may be observed, the latter being a relatively common condi- 
tion. Similar numerical abnormalities occur at the auriculoven- 
tricular valves. Abnormal length or shortness of the leaflets may 
also be observed, or the segments may be united, forming a com- 
plete ring. The latter condition must not be mistaken for the 
agglutination of endocarditis. 

Pathologic Physiology. — Congenital heart-diseases occa- 
sion serious disturbances of the circulation, leading to overfilling 
of the venous channels and often abnormal mixture of the arte- 
rial and venous blood. In consequence of these conditions blue- 
ness or cyanosis is a common symptom, and the terms congenital 
cyanosis and morbus cwmdeus are applied. The imperfect oxida- 
tion of the blood doubtless causes profound effects, but these 



DISEASES OF THE CIRCULATORY SYSTEM. 363 

have not as yet received accurate study. The imperfect circu- 
lation causes certain changes in the tissues, notable among which 




Fig. 158.— Congenital cardiac disease, showing peculiar thickness of lips and nose 

(Eichhorst). 

are thickness of the lips and nose ; giving rise to a peculiar facia! 
expression (Fig. 158) and "clubbing" of the finger-ends (Fig. 




Fig. 159.— Clubbing of the fingers in congenital cardiac disease ; from same case as 
Fig. 158 (Eichhorst). 

159). The blood in congenital cyanosis often contains an excess 
of red blood-corpnscles (see Polycythemia). 



364 



TEXT-BOOK OF PATHOLOGY. 



CIRCULATORY DISTURBANCES. 

Thrombosis of the cavities of the heart results from 
the causes which induce thrombosis elsewhere in the circulatory 
system. These are mainly slowing of the current of blood, some 
roughness or disease of the endocardial lining, and diseased con- 
ditions of the blood itself, which render it more liable to coagula- 
tion. Slowing of the circulation is the most frequent cause of 
intracardiac thrombosis, and leads to the formation of the clots 
found post-mortem in cases of gradual death. If the circulation 
has been slow for a considerable length of time, there may be 
found more or less grayish or white thrombi in the append- 
ages of the auricles or in the ventricles between the muscular 
trabecule, especially near the apex. The formation of these 
is explained by the gradually decreasing rapidity of the current 
of blood, which leads to the deposit of the leukocytes and blood- 
plaques upon the endocardium and their conversion into fibrin. 
The color may be almost completely white ; but if the current is 
almost stagnated, admixture of red corpuscles occurs and pinkish 
or quite red clots (currant-jelly clots) are formed. Of this latter 
sort are the thrombi formed in the heart during the agonal 
period and post-mortem. They are further distinguished from 
the thrombi formed intra vitam by the fact that they are not 
closely attached to the endocardium and between the trabecular 
muscles. 

Among the diseases in which the circulation is prone to be 
sluggish, and which are frequently accompanied by cardiac throm- 
bosis, pneumonia, tuberculosis of the lungs, the asthenic fevers, 
and diseases of the muscle of the heart may be named. Dilata- 
tion of the chambers of the heart and cardiac aneurysm lead to 
thrombosis by their effect upon the rapidity of the circulation 
either in the general heart-cavity in the first, or in the aneurysmal 
dilatation in the second. Among the endocardial lesions which 
occasion thrombosis the most important is acute endocarditis. In 
this condition there is habitually deposited upon the affected part 
of the valves or mural endocardium a capping of fibrin deposited 
from the blood passing over the diseased area. In chronic endo- 
carditis, especially when there are irregular calcareous deposits 
rendering the surface rough and uneven, considerable thrombotic 
deposit may occur. 

Pathologic Anatomy. — Cardiac thrombi, formed some time before 
death, usually appear as deposits upon the heart-wall of a yellow- 
ish or whitish color and rather firmly attached between the muscu- 
lar traDeculse. Occasionally they have a stratified appearance, due 
to the fact that the circulation varied in rapidity during the for- 
mation of the thrombi. Secondary changes are not rare, the 
most striking being softening of the fibrinous mass in places, with 



DISEASES OF THE CIRCULATORY SYSTEM. 



365 




Fig. 160.— Thrombosis in cardiac 
chambers, showing cyst-like struct- 
ure (Orth). 



the formation of cyst-like cavities varying in size from a split pea 
to a cherry (Fig. 160). Sometimes thrombi project from the 
endocardial surface in a polypoid form, 
and these may present the appearance 
of fibroid tumors. A curious form 
occurs in the auricles, the thrombus 
presenting itself as a round mass 
attached to the endocardium by fine 
pedicles or lying entirely free (ball- 
thrombi; globular thrombi). 

Lesions in Other Organs. — Throm- 
bosis of the heart may occasion serious 
disturbance of the circulation by weak- 
ening the heart-muscle or by obstruct- 
ing the valvular orifices. The latter 
is especially common in the case of the 
globular thrombi or the polypoid 
thrombi of the auricles. Passive con- 
gestion of the various organs and the 
secondary changes due to this con- 
dition follow. Thrombosis may lead 
to another and more serious danger, that of embolism. When 
portions of the thrombus are broken off they are carried into the 
circulation and lodge in the small arteries of the spleen, the 
kidney, the brain, the lungs, or elsewhere, causing infarctions, or, 
in case micro-organisms be present in the original thrombus, 
metastatic abscesses and pyemia. 

Thrombosis and Embolism of the Coronary Artery. — 
The former condition is much the more common, as the coronary 
arteries are frequently the seat of advanced atheromatous con- 
traction and roughening, which predispose strongly to thrombosis ; 
and, on the other hand, the mouths of the coronary arteries are 
so placed that emboli are unlikely to enter. The lodgement of an 
embolus seriously compromises the heart's action, as has been 
shown experimentally in animals, and marked pathologic change 
is therefore unlikely to occur before death ensues. When a 
partially obstructing embolus lodges or a thrombus is formed there 
results almost complete anemia of the area supplied by the artery 
affected, and in consequence an anemic infarct. The muscle-fibers 
of the affected area become hyaline or granular, and do not take 
the stain when subjected to ordinary histologic examination. To 
the naked eye the diseased portion presents itself as a white, and 
later as a yellowish, area of softening, and the condition is spoken 
of as myomalacia cordis. It is found most frequently in the 
anterior or posterior wall of the left ventricle, near the apex, from 
the fact that the descending branch of the left coronary artery is 
most commonly involved. Next in frequency to these points the 



366 



TEXT-BOOK OF PATHOLOGY. 



anterior portion of the septum is found to be affected. Small 
areas may heal by absorption of the degenerated tissue, and by 
infiltration and proliferation of connective tissue. In this manner 
a scar is formed, which may remain, or may subsequently lead to 
aneurysmal dilatation. On the other hand, rupture of the heart 
may be occasioned either with or without the formation of an acute 
aneurysmal dilatation at the degenerated area. 

DISEASES OF THE ENDOCARDIUM. 

INFLAMMATION. 

Inflammation of the endocardium, or endocarditis, may be acute 
or chronic, though the latter is in most cases merely a continuation 
of the former. 

Acute endocarditis affects the endocardium of the valves 
in the great majority of cases, but it is sometimes found in the 
endocardium of the cavities of the heart, when it is spoken of as 
mural endocarditis. 

Etiology. — Endocarditis is practically always a secondary pro- 
cess, and is in nearly all, if not all, cases due to the action of 
micro-organisms. Cold and traumatism, upon which the older 
writers insisted as causal factors, act merely as predisposing 
causes. Endocarditis occurs most frequently in association with 
acute articular rheumatism. Next to this cause scarlet fever, 
pneumonia, and puerperal sepsis are most important, but in any 
case of suppurative or infectious disease endocarditis is a possible 
complication. It occurs at times also in Bright' s disease and in 
conditions of great malnutrition, such as carcinoma and certain 
nervous affections. These cases have been cited as opposing the 
view that endocarditis is always infectious and due to micro- 
organisms. It may be that toxic substances resulting from 
improper metabolism act upon the endocardium as do micro- 
organisms, or that portions of the endocardium suffer degeneration 
as a result of depressed nutrition, but it is also possible that ter- 
minal or intercurrent infection from some hidden source may occur 
in these chronic diseases, with resulting endocarditis. 

As to the micro-organisms themselves, the most important are 
the Staphylococcus pyogenes aureus, the Streptococcus pyogenes, and 
the Diplococcus pneumoniae. But there are many forms which 
have been less frequently detected. Among such are the Staphy- 
lococcus pyogenes albus, the Micrococcus endocarditidis capsulatus 
and rugatus, the Bacillus endocarditidis griseus and capsulatus, 
Bacillus pyogenes foetidus or Bacillus coli communis, the Bacillus 
diphtherias, and the bacillus of typhoid fever. The tubercle- 
bacillus has been found in a few cases, but it is generally believed 
that its presence is explainable as a secondary deposit rather than 



DISEASES OF THE CIRCULATORY SYSTEM. 



367 



as the cause of the endocarditis. Recently the gonococcus has 
been recognized as one of the organisms capable of causing endo- 
carditis. 

The micro-organisms reach the point of disease from the blood 
passing over the endocardium, and not through the coronary cir- 
culation. This is proved by the fact that the aortic and pulmo- 
nary leaflets are frequently involved, and they are not supplied 
with blood-vessels, and also by the experimental production of 
endocarditis by injections of micro-organisms into the blood after 
the valve has been mechanically injured. In such cases there is 
a direct deposit of micro-organisms upon the heart-valves. 

Pathologic Anatomy. — It was customary formerly to distinguish 
two varieties, a simple or verrucose, or benign endocarditis, and an 
ulcerative, septic, mycotic, diphtheritic, or malignant form; but it 
seems unnecessary at the present time to maintain strictly such a 
distinction. The cases vary in anatomical appearance and in 
malignancy, but there is no essential difference and no sharp 
dividing-line. 

The most common seats, in order of frequency, are the mitral 
valve, the aortic valve, the pulmonary valve, and the endocardium 
of the left ventricle, the left auricle, and the right ventricle. The 
part of the valves first involved is a line running across the leaf- 
let at about a distance of 2 mm. from the free edge. It is along 
this line that the valves impinge in closing, and it is probable 
that the mechanical injury sustained predisposes to endocarditis. 
In the cavities the lesions are frequently found upon the chordse 




Fig. 161.— Section through a segment of the aortic valve and adjacent parts of the aorta 
and heart, showing vegetations on the aortic valve (magnified) : b, aortic valve segment ; 
c, c, vegetations ; /, calcareous particles in the base of the aortic valve (Bramwell). 

tendinese, and of the parts of the mural endocardium proper most 
apt to be affected may be mentioned the portion of the left ven- 
tricle near to the septum and the aortic valves, and the endocar- 
dium of the left auricle on the posterior and outer wall above 
the posterior mitral leaflet. 



368 



TEXT-BOOK OF PATHOLOGY. 



The first appearance of endocarditis is that of an area of opacity 
or slight roughness extending in a line across the valve or involv- 
ing the endocardium elsewhere. Later, small nodular elevations, 
not unlike a row of small beads, may form ; and finally there is a 
distinct, irregular, and wart-like fibrinous elevation (Fig. 161). To 
cases of this character the name verrucose endocarditis has been 
given; or from the usually benign character, the name simple 
endocarditis ; or from its most frequent cause, rheumatic endo- 
carditis. In other cases the mass of fibrinous deposit is more 
abundant (Fig. 162) and more irregular, while in still others the 




Fig. 162. — Endocarditis of the aortic and mitral valves, showing vegetations (fibrin- 
deposits; of considerable size (Kast and Rumpel). 

deposit of fibrin does not take place, or, if so, is soon detached, 
while necrotic changes occur in the endocardium, leading to the 
formation of irregular ulcers. Secondary deposits of fibrin may 
cover an ulcer after its formation, or its edges may be heaped 
with fibrin ; and not rarely the active necrotic process in the 
endocardium is not visible until the fibrinous coating, which is 
usually considerable in such cases, is removed. These forms of 
endocarditis are those that have been termed malignant, diph- 
theritic, septic, mycotic, or ulcerative. They are especially frequent 
after puerperal sepsis or other septic diseases and in pneumonia, 
but there is no well-established dividing-line between the benign 
cases and the severe cases, either in etiology, in morbid anatomy, 
or in the clinical course and termination, so that I prefer to re- 
gard them as varying grades of the same general process. 

Microscopically the endocardium beneath the coat of fibrin 



DISEASES OF THE CIRCULATORY SYSTEM. 



369 



shows desquamation of the endothelial cells, with frequently some 
hyaline degeneration or coagulation-necrosis of the latter. Below 
this there are round-cell infiltration and, as the process continues, 
proliferation of fibroblastic cells. The fibrinous covering of the 
valve itself consists of flakes or granular masses, or a fibrillar net- 
work. By the proper staining-methods masses of bacteria may 
frequently be demonstrated in the superficial layers of the endo- 
cardium or in the fibrinous deposit. 

The simple differs from the malignant forms of endocarditis 
merely in the lesser activity of the necrotic changes in the endo- 
thelium and the greater prominence of reparative processes (round- 
cell infiltration, proliferation of connective tissue). 

Results. — Simple endocarditis may be healed by the gradual 
absorption or breaking off of the fibrinous deposit and its dis- 
semination in the circulation, with coincident thickening of the 
endocardium at the point of disease by the formation of fibro- 
blastic cells and sclerotic connective tissue. When the process 
is very limited, and especially when the mural endocardium 
is affected, merely a white spot of thickening on the endo- 
cardium results. When the process is deep there may be 




Fig. 163.— Aneurysm of the mitral valve, with rupture of the valve-cusp, seen from 
the auricular surface : a, wall of left auricle ; b, anterior segment of the mitral valve, the 
chordae tendinese have been cut short ; c, aneurysm with triangular opening (Bramwellj. 

decided distortion by contraction of the new-formed connective 
tissue. When the deposit of fibrin is large it frequently under- 
goes calcification, and remains as an irregular, calcareous mass 
attached to the valve. In the severer or malignant cases destruc- 
tion of an entire valve or of one of the chordae tendinese may 
occur. When one of the layers of the valves alone is penetrated 

24 



370 



TEXT-BOOK OF PATHOLOGY. 



acute valvular aneurysm may be formed by a pouching of the 
other layer of the valve (Fig. 163). 

Mural endocarditis of malignant type may lead to myocarditis 
of a purulent character, and may even penetrate to the pericardium 
and set up a purulent pericarditis. 

Lesions in Other Organs. — The most serious danger of endo- 
carditis is embolism. Small fragments of the fibrinous deposits 
are liable to be carried off into the peripheral circulation, and in 
ulcerative cases fragments of the valves themselves may be so con- 
veyed. They are prone to lodge in the arteries of the spleen, 
kidneys, and brain, forming hemorrhagic infarcts or metastatic 
abscesses, according to the non-infective or infective character of 
the embolus. 

Chronic Endocarditis usually affects the valves of the heart 
and leads to the distortions of the valves constituting chronic 
valvular heart disease. Clinically, there are signs of disturbances, 
and eventually more or less complete failure of the circulation. 

Etiology. — Chronic endocarditis may be merely the continuation 
of acute endocarditis, or it may occur as an insidious process, 
chronic from the outset. In the former group of cases the causes 
are, of course, those of acute endocarditis, and it is particularly 
the rheumatic form that is likely to pass on to a chronic condition. 
The severer grades, or those commonly spoken of as malignant 
endocarditis, are usually fatal, though occasionally they may termi- 
nate by reparative overgrowth of fibrous tissue. The group of 
cases in which the disease is chronic from the start has much in 
common with arteriosclerosis and atheroma, as far as etiology is 
concerned. These cases occur more frequently in persons of 
advanced years and in those whose occupation has been laborious. 
Chronic alcoholism, gout, lead-poisoning, syphilis, and diabetes are 
among the recognized causes. Not rarely the endocardial disease 
is secondary to the arteriosclerosis, and it may be directly due to 
it, resulting from the constant elevation of blood-pressure due to 
that disease. Laborious occupations act in a similar manner. 

Pathologic Anatomy. — In brief, the changes that occur in the 
endocardium are overgrowth of fibrous tissue, causing thickening 
with subsequent contraction and distortion of the valves. The 
chordae tendinese are frequently involved and become converted 
into sclerotic cords of a whitish color, and less frequently white 
elevations are seen upon the mural endocardium. 

Microscopically there are found the characteristic appearances 
of new-formed connective tissue with occasionally, in the earlier 
stages, the appearances of granulation-tissue. New-formed blood- 
vessels may be found within this tissue, though frequently these 
are degenerated (hyaline and obliterated). Subsequently other de- 
generations take place. The area of thickening becomes more 
translucent and hyaline, then opaque and soft ; coagulation-necrosis 



DISEASES OF THE CIRCULATORY SYSTEM. 371 



and fatty degeneration take place, and there may thus be formed 
beneath the endocardial surface a lesion somewhat resembling a 
minute abscess. This may rupture upon the endocardial surface, 
forming a so-called atheromatous ulcer, upon which fibrinous 
deposits may collect ; or it may be slowly inspissated and con- 
verted into a calcareous patch. In cases in which acute endo- 
carditis with thrombotic deposits passes into chronic endocarditis 
the fibrinous masses of the surface may be rendered calcareous at 
the same time that the sclerotic processes are taking place in the 
valve. Subsequently the same degenerative changes and calcifi- 
cation may occur in the tissue of the valve itself, as are seen in 
the atheromatous form of the disease. In the late stages it is 
often quite impossible to determine whether the case began as an 
acute endocarditis, or whether it was chronic from the first. 

The segments of the valves are frequently greatly shortened 
and rounded, so that they become mere stumps, or they may be 
curled upon themselves or drawn back and firmly adherent to the 
wall of the aorta, pulmonary artery, or the ventricular cavity. 
The individual segments may be agglutinated and united as a ring 
or diaphragm projecting from the valvular orifice. 

The valvular function is interfered with in two ways : first, 
obstruction may be offered to the outflow of blood by the rigid pro- 
jecting valves, a condition to Avhich the term stenosis is applied ; 
or, on the other hand, the valves may be so distorted, shortened, 
or drawn backward that they are no longer able to close, and in- 
sufficiency results. The semilunar valves are particularly prone to 
be shortened and thickened and recurved, and insufficiency is 
therefore most likely to occur. The mitral valve is frequently 
thickened and converted into a funnel-like formation by agglutina- 
tion of the edges of the anterior with those of the posterior segment. 
There may thus be merely a slit-like orifice (button-hole mitral), 
which occasions great obstruction to the outflow of blood from the 
auricle. Somewhat similar changes are met with at the tricuspid 
valve. The pulmonary valve is rarely affected in later life, but is 
sometimes the seat of fetal endocarditis, leading to permanent 
changes. 

Resulting Changes in the Heart. — The valvular defects can be 
overcome in only one way — by increase of the power of the heart- 
muscle. Hypertrophy is therefore the natural result. This affects 
first the cavity upon which excessive work falls as the result of 
the regurgitation of blood in cases of insufficiency, or as the result 
of the excessive strain placed upon the heart- wall to force the blood 
through the narroAved orifice in stenosis. The amount of hyper- 
trophy varies with the condition of the general health of the indi- 
vidual and with the seriousness of the heart-lesion itself. When 
the general health is good there is apt to be commensurately ade- 
quate hypertrophy, and when the lesion is not of sufficient gravity 



372 



TEX1-B00K OF PATHOLOGY. 



to interfere with the circulation in the coronary arteries, and the 
heart is therefore constantly supplied with a sufficiency of blood, 
hypertrophy is well maintained. Eventually as the result of con- 
tinued overwork and of continuously increasing embarrassment of 
the circulation or of intercurrent diseases, the heart-muscle suffers 
fatty or fibroid degeneration, the cavities dilate, and the circulation 
fails. 

Changes in Other Organs. — The passive congestions result- 
ing from failure of the muscle of the heart are often extreme, and 
may lead to profound changes in various organs, notably the lungs, 
liver, and kidneys. These are discussed in the appropriate sections. 
Embolism is a not infrequent accident in chronic endocarditis, the 
emboli being parts of the valvular deposits or parts of thrombi in 
the cavities of the heart. 

Pathologic Physiology. — Endocarditis, acute and chronic, 
leads to various disturbances of the circulation and of the general 
health. In acute endocarditis the lesions may become the center 
of dissemination of infectious material, and the disease may run 
its course with all the manifestations of an obscure septicemia. 
This is particularly true of the cases usually designated as malig- 
nant. Serious disturbance of the heart-action occurring in acute 
cases is sometimes difficult to explain. The lesions upon the 
valves may be seemingly very insignificant, and yet the heart may 
be very irregular in action and exceedingly weak. In part this 
may be reflex and in part it is probably the result of associated 
disease of the myocardium. Some recent investigations, made 
according to modern methods, have shown the heart-muscle impli- 
cated more often than has been suspected. Acute myocarditis and 
diseases of the blood-vessels of the myocardium (thrombosis) have 
been discovered. 

Chronic endocarditis (valvular disease) occasions more or less 
profound mechanical disorders of the circulation. The severity 
of these depend upon the condition of the heart-muscle more than 
upon the severity of the valvular lesion. There is always a ten- 
dency to compensatory hypertrophy of the heart -muscle, and for a 
time this may suffice to avert serious disturbances ; but with 
hypertrophy there is always degenerative change (fibrous myocar- 
ditis, and later fatty degeneration), as a result of which the cardiac 
power eventually fails, and symptoms of venous congestion de- 
velop. The degree of hypertrophy and of degeneration depends 
upon the nature and severity of the valvular lesion, upon the age 
and general condition of the individual, and upon associated local 
conditions, such as disease of the coronary artery. 

When compensation fails, the various organs of the body suffer 
congestion. The lungs are first affected in disease of the left 
heart (mitral and aortic disease). The capillaries of the pul- 
monary alveoli become over-full, and encroach upon the lumen of 



DISEASES OF THE CIRCULATORY SYSTEM. 373 



the alveoli, or by elongation stretch the alveolar walls and render 
them inelastic. In either case proper respiration is prevented — a 
condition which is further aided by the retarded pulmonary circu- 
lation. As a result of these conditions, dyspnea (cardiac asthma), 
cough, and expectoration develop. In extreme cases edematous 
exudation takes place, and in long-continued cases cyanotic in- 
duration of the lung occurs. In such instances there may be con- 
tinuous cough and respiratory insufficiency. 

When the right heart fails, the liver, spleen, gastro-intestinal 
mucosa, the kidneys, and the peripheral circulation suffer conges- 
tion. The liver may become greatly engorged, and in certain 
cases (tricuspid regurgitation) actually pulsates with each ventricu- 
lar systole. The swollen liver-cells and the engorged vessels 
cause obstruction of the biliary capillaries, and consequently pro- 
duce jaundice. To some extent this may be due to associated 
congestion of the biliary channels. Congestion of the gastro- 
intestinal mucosa may occasion various forms of gastric or intesti- 
nal derangement. 

Metabolic disturbances of various sorts may occur in con- 
sequence of the imperfect circulation. The respiratory exchange 
of gases, in some cases at least, is reduced, though the degree of 
cyanosis cannot be taken as an index of the reduced oxidation. 
In man cyanosis is dependent upon stagnation of circulation 
rather than reduced oxidation. The products of metabolism 
excreted in the urine may indicate the reduction in oxygen in 
the tissues. The metabolic consumption of the proteids of the 
body seems to be increased, but the explanation of this fact has 
not yet been satisfactorily determined. Some regard it as a con- 
sequence of molecular necrosis due to insufficiency of the supply 
of oxygen. The excretion of nitrogenous elements may, however, 
be reduced when transudates are forming. This is due to the 
storing up of metabolic products in the transudates. The urine 
may present albumin as a result of chronic congestion and second- 
ary renal disease ; the hepatic functions are disturbed by congestion 
and jaundice may result ; and in the more severe instances hydro- 
bilinuria occurs. The condition of* the blood is of special inter- 
est. During periods of failing compensation the concentration of 
the blood is increased or normal, and the number of blood-corpus- 
cles may be excessive. In part, at least, these conditions are 
explained by the assumption that the corpuscles are retained in 
the peripheral parts of the circulation in greater measure than the 
fluid elements (see Polycythemia). When the cardiac compensa- 
tion is well maintained some anemia may be apparent, especially 
in cases of aortic disease. 

Disturbance of the rate or rhythm of the heart is not infrequent. 
The rate is usually more rapid, but in aortic stenosis it is slow. 
This is a conservative process, as it enables the ventricle to dis- 



374 



TEXT-BOOK OF PATHOLOGY. 



charge its contents through the narrowed orifice. Arrhythmia is 
generally proportioned to the grade of degeneration of the muscle 
of the heart, and is especially marked in cases in which the walls 
of the auricles are involved. The attempt to connect disorders of 
rhythm with disease of the intracardiac nervous mechanism has 
thus far failed of demonstration. 

CIRCULATORY DISTURBANCES. 

Anemia of the heart-muscle may be part of a general 
anemia. It may occur in cases of narrowing or obstruction of 
the coronary arteries, and it may be the result of the pressure of 
pericardial effusions. When long continued it leads to fatty 
degeneration of the heart, but is itself of little consequence. 

Hyperemia of the heart-muscle may occur when there is 
obstruction to the return of the blood to the right heart through 
its venous channels. It may be part of a general hyperemia in a 
failing compensation of valvular or muscular diseases of the heart. 
The heart-muscle assumes a dark-red color, and the veins are seen 
under the epicardium as dilated bluish vessels. 

Hemorrhages in the heart-muscle may result from ob- 
struction of the coronary arteries, when the hemorrhage assumes 
the form of an infarct. There may also be hemorrhages in cases 
of intense myocarditis or surrounding abscesses of the heart-mus- 
cle, and finally points or streaks of hemorrhagic infiltration may be 
seen between the muscle-fibers in persons who have died with 
some form of hemorrhagic diathesis, from sepsis, or from various 
intoxicants. 

DEGENERATIONS. 

Parenchymatous degeneration, or cloudy swelling of the 
heart, was designated by Virchow as parenchymatous myocarditis. 
It is essentially a degenerative process and should be so described, 
though it forms a not inconsiderable part of the pathologic changes 
occurring in the heart in acute myocarditis. 

Etiology. — The immediate cause is infection. It is met with 
in the course of diphtheria, typhoid fever, scarlet fever, rheuma- 
tism, and other infections. It may be that elevation of the tem- 
perature alone suffices to bring it about, and in these cases no 
doubt abnormal substances resulting from disordered metabolism 
are the direct toxic agents, but, as a rule, it is the specific toxin of 
the infections that occasions the myocardial disease. Localized 
parenchymatous degeneration may be found in the heart-fibers ad- 
jacent to areas of endocarditis or pericarditis, and doubtless the 
same etiologic factors are at work in this as in more generalized 
instances. 

Pathologic Anatomy. — The changes are more marked in the left 
ventricle than elsewhere ; though any part of the heart may be 



DISEASES OF THE CIRCULATORY SYSTEM. 



375 



affected. As a rule, parenchymatous degeneration occurs as a 
diffuse process, but there may be only limited areas here and 
there. The myocardium becomes pale in color and often has a 
turbid appearance ; it is softer than normal, the heart-walls are 
usually flabby, and the cavities somewhat dilated., Microscop- 
ically, the fibers are found to be filled with fine granules of albu- 
minous nature, which may completely obscure the striations and 
even the nuclei, but which may be cleared up by the addition of 
acetic acid. Multiplication of the nuclei and round-cell infiltra- 
tion of the intermuscular connective tissue may be observed, but 
these are inflammatory changes rather than degenerative, and are 
not, therefore, strictly a part of the disease in question. Paren- 
chymatous degeneration may be complicated by a form of hyaline 
degeneration, the affected fibers becoming converted into cylin- 
ders of waxy appearance. When cloudy swelling persists fatty 
degeneration is often the terminal change. 

Amyloid degeneration results from the causes which induce 
amyloid disease in other organs. It is not infrequently found in 
minute areas here and there, but only rarely has it been seen as a 
widespread process affecting the connective tissue between the 
muscle-fibers and beneath the endocardium and pericardium. In 
such cases the same wax-like appearance is seen as in the liver or 
spleen, and the characteristic reaction with iodin may be demon- 
strated. 

Hyaline degeneration is sometimes associated with amy- 
loid, and gives rise to a glassy or waxy transformation of the con- 
nective tissue. It is usually seen in small areas, but may be quite 
widespread. Zenker described a form of hyaline disease of the 
muscle-fibers themselves as occurring in typhoid and other infec- 
tious fevers, and affecting the heart-muscle as well as the muscles 
of the abdominal wall. This is usually associated with parenchy- 
matous degeneration and occurs in limited areas. Microscopically 
there may be seen small hyaline masses or globular areas embedded 
in the muscle-fiber, the rest of the fiber snowing the appearances 
of cloudy swelling. 

Fatty infiltration, or obesitas cordis, is but an increase 
of the normal condition. In the normal heart there is a certain 
amount of fatty deposit beneath the epicardium, especially in the 
furrows and along the lines of the blood-vessels. In disease this 
may become enormously increased and there may be penetration 
of the adipose tissue into the wall of the heart between the mus- 
cle-fibers, sometimes as far as the subendocardial fibrous layer. 

Etiology. — The causes are those which induce general obesity. 
Thus, it may be the consequence of an hereditary tendency or 
sedentary habits, with overeating and drinking ; it is more com- 
mon in advanced years than in early life. V*ery frequently it is 
met with in women who have grown stout at the menopause ; 



376 



TEXT-BOOK OF PATHOLOGY. 



sometimes, however, considerable deposit about the heart may 
occur in persons otherwise presenting no tendency to fatness. 

Pathologic Anatomy. — The adipose tissue beneath the visceral 
pericardium may be slightly increased in amount, or the heart may 
be embedded within an enormous deposit of fat, which may involve 
not alone the epicardium, but the parietal layer and the medias- 
tinum as well. On section through the heart-wall, trabecular of 
adipose tissue may be seen passing through the heart's substance, 
and sometimes subendocardial deposits may be seen as a uniform 
infiltration beneath the endocardium or as localized deposits pro- 
jecting into the heart beneath the endocardium. Microscopically 
fatty infiltration presents the ordinary appearances of adipose cells 
lying between the heart-muscle fibers (Fig. 164). The fibers 
themselves are not involved ; but they may become atrophic from 




Fig. 164.— Fatty infiltration of the heart, from a section through the wall of the right 
auricle (Bramwell). 

pressure, and in such instances present a more yellowish or brown- 
ish color than normal, and microscopically show an abundance of 
granules. In other cases pronounced fatty degeneration is seen in 
the muscle-fibers. 

Results. — Weakening of the heart-muscle must necessarily 
result from the mechanical impediment imposed upon the muscle. 
Circulatory disturbances are therefore met with as in valvular 
disease or fatty degeneration. Occasionally rupture of the heart 
occurs, and is due to the atrophic condition of the muscle proper 
and a want of resisting power of the infiltrating adipose tissue. 
It is especially prone to occur when the disease is localized. 

Fatty degeneration affects the muscle-fibers themselves. 

Etiology. — Fatty degeneration results from malnutrition or 
from toxic agencies. The most frequent cause is anemia, either 



DISEASES OF THE CIRCULATORY SYSTEM. 377 



local or general. Local anemia is due to sclerosis and narrowing 
of the coronary arteries ; or it may be the consequence of improper 
circulation in the coronary vessels attending the final stages of 
valvular disease of the heart. Fatty degeneration is therefore a 
terminal condition in arterial sclerosis affecting the coronary ves- 
sels and in valvular disease. The remote or antecedent causes 
are those which bring about arteriosclerosis. We find it therefore 
in elderly persons of the male sex who have had syphilis, who 
have used alcohol excessively, or have gout or chronic Bright's 
disease. The fatty degeneration of the heart resulting from gen- 
eral anemia is most typically seen in pernicious anemia, in which 
the most extreme grades of fatty disease are sometimes witnessed. 
Of the cases which are due to toxic agents we may distinguish 
those resulting from specific infections and those occurring in 
various chemical intoxications. In the specific fevers, in which 
intense parenchymatous degeneration occurs, and among these 
diphtheria is most prominent, fatty degeneration is sometimes the 
terminal condition. Among the external poisons capable of 
producing the disease phosphorus and arsenic are important. 

Pathologic Anatomy. — Fatty degeneration may be a localized 
or a diffuse process. As a rule, a considerable portion of the 
heart is affected, but only isolated fibers or groups of fibers are 
involved. There results a somewhat speckled or mottled condi- 
tion, which is especially visible beneath the endocardium. Streaks 
or lines of a yellowish or whitish color alternate with the darker 
portions of normal muscle. When the process is uniform the 
entire muscle assumes a yellowish hue. It is softer than normal, 
the cavities tend to dilate, and the walls may be considerably 
thinner than normal. 

Microscopically the muscle-fibers are found to be filled with 




Fig. 165.— Fatty degeneration of the heart in a case of pernicious anemia ; some of the 
fibers in the lower part of the illustration are normal (Birch-Hirschfeld). 

small granules of a dark color or with small droplets of high 
refractive power (Fig. 165). These may completely obscure the 
nucleus, or they may be arranged in groups at the poles of the 
nucleus. Sometimes distinct vacuolization of the fibers is seen, 
especially in cases in which fibroid myocarditis accompanies the 



378 



TEXT-BOOK OF PATHOLOGY. 



fatty change. The nature of the granules and droplets within the 
fibers is well demonstrated by treating the section with osmic acid, 
w T hen the fat-droplets become intensely black. 

Associated Conditions. — In cases of coronary sclerosis, or valvu- 
lar heart disease with failure of compensation, fatty degeneration 
is rarely the sole pathologic condition. As a rule, fibroid myo- 
carditis accompanies it, and the latter may be the more extensive 
and important condition of the two. Fatty infiltration is often 
met with as an associated condition, and may be the direct cause 
of the degeneration by the pressure exerted upon heart-muscle 
fibers by the infiltrating fat. Rupture of the heart may occur in 
cases in which fatty degeneration affects localized areas, as is often 
the case near the apex of the heart. 




Fig. 166.— Marked general segmentation with great diastasis of the pieces ; X 120 (from 

the American Journal of the Medical Sciences) (Hektoen). 

Segmentation of the Fibers. — This is an interesting con- 
dition occasionally observed, especially in cases in which sudden 
death has taken place. It consists in a transverse splitting of the 
fibers, by which they are converted into columns of varying length 
separated by transverse fissures (Fig. 166). It has been described 
under the name of Hat segmentaire, or myoeardite segmentaire, by 
French writers. A considerable discussion as to its significance 
has arisen, some holding that it is a condition of clinical as well as 
pathologic importance ; others, that it occurs during the death- 
agony or post-mortem. Whether the latter statement be true or 
not, the segmentation seems to indicate a degree of fragility of the 
fibers, and in particular of the cement-substance, wholly abnormal, 
though it may not be demonstrable by our present means of exam- 



DISEASES OF THE CIRCULATORY SYSTEM. 379 



ination. This fragility may be due to digestive action of bacteria 
or bacterial products, as has been suggested. 

Degeneration of the intracardiac ganglia has been 
noted by a number of observers in myocarditis and in cases of 
angina pectoris without gross cardiac alteration. The changes 
observed are swelling, or granular, fatty, and hyaline degeneration 
of the ganglion-cells, and infiltration of round cells with sclerotic 
formation between the nerve-cells. The importance of these 
changes has not been determined. 

Pathologic Physiology. — The functional disorders in de- 
generations of the myocardium may be due to the direct injury of 
the fibers, or to disturbances of the nervous mechanism of the 
heart. The latter seems to be the case in instances in which 
marked cardiac irregularity, or arrhythmia, occurs. The disease 
of the fibers explains the weakness of the heart-action ; and this is 
especially marked in cases (of fatty and fibroid disease) in which 
the circulation through the coronary arteries is insufficient. Recent 
investigations have shown that fatty degeneration of the heart- 
muscle in itself causes much less cardiac weakness than has 
generally been supposed. Sometimes the heart is arrested and 
sudden death occurs in cases of myocardial degeneration due to 
infectious fevers (diphtheria). This was formerly ascribed to 
heart-clots, but is now recognized as a form of sudden and com- 
plete asystole due to the myocardial disease or to associated nervous 
disorders, organic (in the intracardiac ganglia or in the cardiac 
nerves) or reflex. The disturbances of the general circulation in 
myocardial disease and their results are similar to those met with 
in valvular disease. (See also pathologic physiology of Fibroid 
Degeneration of the Heart.) 

INFLAMMATION. 

Inflammation of the heart-muscle, or myocarditis, may be either 
acute or chronic, diffuse or circumscribed. 

Acute myocarditis was designated carditis by the older 
writers, though the same term was applied to endocardial and 
pericardial inflammations as well. It may be circumscribed or 
diffuse, the former appearing in the form of abscesses of the 
heart-muscle. 

Acute circumscribed myocarditis, or abscess of the heart, 
may occur in connection with penetrating endocardial lesions or in 
association with pericarditis. More frequently the infection takes 
place through the coronary circulation, and the metastatic abscesses 
of the heart are but a part of a general pyemic disease (Fig. 167). 
This occurs in cases of puerperal sepsis, in osteomyelitis, and other 
intensely septic diseases, but particularly in cases of malignant 
endocarditis. 



380 



TEXT-BOOK OF PATHOLOGY. 



Pathologic Anatomy. — When the infectious emboli are large a 
single abscess or a few abscesses result, while in cases of finely 
disseminated infectious particles the heart-substance may be 
studded with innumerable suppurating points. These are more 
common in the left ventricle and in the anterior wall than else- 
where. At first the lesion may present itself as a minute, hemor- 
rhagic, or necrotic area, but soon the focus softens and forms a 
purulent collection. In size the abscesses vary from the merest 
points to cavities the size of a cherry, and as much as an ounce of 
pus has been removed from a single cavity. Perforation may take 
place into the heart itself, and acute cardiac aneurysm or even 
rupture of the heart may ensue. On the other hand, the abscess 
may discharge into the pericardial sac, or without such rupture 
may set up purulent pericarditis. Occasionally the pus becomes in- 




FlG. 167.— Embolic abscess of the myocardium (Karg and Schmorl). 

spissated and fibrous overgrowth causes its complete encapsulation, 
or finally the area may be rendered calcareous. Such terminations, 
however, are rare, the patient usually perishing of the pyemic pro- 
cess, as a part of which the abscesses in the heart occur. 

In suppurative myocarditis occurring from extension in conse- 
quence of malignant endocarditis communicating sinuses may be 
established between the chambers of the heart. 

Acute diffuse myocarditis occurs in various forms of infec- 
tious fevers. It was first recognized in typhoid fever, but is more 
common in diphtheria and scarlet fever, and is met with in acute 
rheumatism, puerperal septicemia, and various other infections. 
It is most likely that the toxins of the infectious diseases named 
are the immediate causes, and not the specific bacteria themselves. 
The process may be entirely diffuse, but in most cases the left 
ventricle is more seriously involved than other parts, and often 



DISEASES OF THE CIRCULATORY SYSTEM. 



381 



there are merely localized areas of myocarditis scattered about in 
various parts of the ventricular wall. 

Pathologic Anatomy. — The affected heart-muscle is soft and 
often distinctly friable. In the earlier stages there may be spots 
of hemorrhagic infiltration;, but as a rule the color is rather lighter 
than that of the normal organ. It may be noticeable that the 
bundles of fibers easily separate from one another. The cavities of 
the heart are frequently dilated, particularly the left ventricle. 

Microscopically the important changes are diffuse infiltration of 
round cells in the connective tissue between the muscle-fibers (Fig. 
168), and proliferation of the connective tissue itself, with forma- 




Fig. 168.— Acute diffuse myocarditis. 



tion of rounded or spindle-shaped fibroblastic cells. There is no 
tendency to suppuration. The blood-vessels are usually somewhat 
distended with blood, and there may be distinct proliferative thick- 
ening of their walls. Degenerative changes of the muscle-fibers 
themselves are rarely, if ever, absent, and it is most probable that 
the first stage in the process is a toxic degeneration of the muscle- 
fibers, and that the intermuscular infiltration and proliferation are 
consequent upon the primary degeneration. The fibers become 
granular and opaque, the striations are indistinct; occasionally 
there may be vacuolization, and sometimes the segmentation to 
which so much attention has been directed of late. Proliferation 
or swelling of the nuclei of the muscle-fibers is frequent, and the 
hyaline transformation of Zenker is sometimes observed. 

Results. — Under entirely favorable conditions acute, diffuse, 
and non-suppurative myocarditis usually terminates in complete 
resolution. It is, however, quite likely that the proliferative 
changes noted in the intermuscular connective tissue often ad- 
vance to complete organization and formation of localized areas 
of sclerosis. Death from dilatation of the cavities and cardiac 
failure is not uncommon. 



382 



TEXT-BOOK OF PATHOLOGY. 



Chronic myocarditis, or fibrous myocarditis, like the acute 
form, may be diffuse or localized, though iu this case the circum- 
scribed form is the more common. 

Etiology. — It is not unlikely that many cases are consequent 
upon acute diffuse myocarditis, as has been already suggested. 
In such cases the myocarditis may be looked upon as a pri- 
mary affection. More commonly the process is secondary, and is 
dependent upon primary disease of the coronary arteries or dis- 
turbances of the circulation in the coronary arteries. It is there- 
fore very common to find areas of sclerosis in cases of atheroma of 
the coronary arteries or in valvular disease of the heart in which 
the coronary circulation has finally become deficient. Among the 
remote antecedent causes are the conditions which are prone to 
occasion arteriosclerosis, such as old age, alcohol, gout, syphilis, 
and the like. The connection between the arterial disease and the 
resulting myocardial sclerosis has been the subject of considerable 
dispute. No doubt, in some instances, the circumscribed areas of 
fibrous overgrowth met with in the distribution of branches of the 
coronary artery represent the scars of healed infarctions. In other 
cases, however, it would seem more likely that a slow degenerative 
change with gradual overgrowth of the connective tissue occurs in 
consequence of the disturbed circulation through the damaged 
coronary vessels, and it has been urged that in these instances the 
fibroid disease of the heart is degenerative, and not in reality an 
inflammatory process at all. Diffuse sclerosis may be associated 
with hypertrophy in cases of valvular disease and other conditions 
causing cardiac enlargement. Dehio has suggested that fibroid 
degeneration or myofibrosis is a conservative process designed to 
strengthen a heart-wall that has become impaired by some de- 
generation or functional weakness, just as, according to Thoma, 
the fibrous nodules in atheroma serve to strengthen parts of the 
arterial wall that have become weakened by disease of the muscu- 
laris. 

Localized myocarditis with fibroid overgrowth is very com- 
monly met with at the tips of the papillary muscles in association 
with chronic endocarditis and disease of the chordae tendinea?. 

Superficial myocarditis of a fibroid character may be seen 
beneath the pericardium or endocardium which has been thick- 
ened by chronic inflammation. 

Pathologic Anatomy. — The characteristic change is the forma- 
tion of sclerotic areas in the muscle-substance. These appear 
either as more or less irregular spots, or as streaks or lines running 
in the direction of the fibers of the heart. They are most com- 
mon in the anterior wall of the left ventricle, near the apex, in the 
septum, and at the tips of the papillary muscles ; but the entire 
substance of the heart may be involved and thickening of the walls 



DISEASES OF THE CIRCULATORY SYSTEM. 383 



may result. The impediment offered to the muscle of the heart 
by the intermuscular sclerosis may lead to true hypertrophy, but 
more commonly there is degeneration of the fibers in consequence 
of the pressure of the new-formed tissue, and yellowish areas of 
fatty degeneration are frequently observed. 

Microscopically the diseased areas are found to consist of more 




Fig. 169.— Edge of an area of fibrous myocarditis, showing replacement of the fibers by- 
connective tissue (Orth). 

or less well-organized connective tissue lying between the muscle- 
fibers and pressing them far apart, or taking the place of atrophic 
muscle-fibers (Figs. 169 and 170). 




Fig. 170.— Chronic myocarditis, showing extensive destruction of fibers. 

Sometimes certain portions show the earlier stages of the 
process, round-cell infiltration and proliferation of the connective 



384 



TEXT-BOOK OF PATHOLOGY. 



tissue being the important features (Fig. 171). As a rule, how- 
ever, the diseased areas are found in a completely organized con- 




Fig. 171— Endomyocarditis, showing, a, thickened endocardium ; b, bands of muscle- 
fibers with interstitial infiltration of round cells and proliferated connective tissue 
(Bramwell). 

dition. The muscle-fibers themselves suffer granular and fatty 
degeneration, and not infrequently distinct vacuolization is ob- 
served. 

Results. — In cases in which a considerable area of chronic 
myocarditis is developed, as is not uncommonly observed at the 
apex in consequence of thrombotic or embolic obstruction of the 
anterior coronary artery, an aneurysm of the heart may result 
from gradual stretching of the fibroid area. In cases in which the 
process is diffuse the heart-muscle may at first undergo hyper- 
trophy in consequence of the excessive labor imposed upon it, but 
eventually degeneration from pressure upon the fibers gains the 
ascendency, dilatation of the cavities ensues, and general failure 
of the circulation is the terminal result. 

It is not unusual to find diffuse arteriosclerosis and fibroid 
disease of other organs associated with chronic myocarditis. In 
such cases the antecedent cause is the arterial disease, which in 
turn may be dependent upon some systemic disorder. 

Pathologic Physiology. — The immediate effect of chronic myo- 



DISEASES OF THE CIRCULATORY SYSTEM. 



385 



carditis or fibroid degeneration of the heart is a loss of power. By 
some it has been held that the fibroid tissue is designed as a sup- 
port for the heart-muscle weakened by other causes, such as de- 
generation of the muscle-fibers themselves, just as it has been 
claimed that nodules of arteriosclerosis are intended as support 
for areas of weakness of the muscular layers of the arterial walls. 
This theory is not generally accepted ; but, on the other hand, it 
is certain that the presence of fibrous tissue weakens the heart so 
far as its proper function (contractility) is concerned. For a time, 
hypertrophy of the muscular elements may counterbalance the 
functional weakness occasioned by the fibroid change, but event- 
ually the muscle fails, and this failure is usually hastened by fatty 
degeneration and atrophy of the muscle-fibers, which in turn are 
doubtless occasioned by the fibroid change, especially that 
involving the walls of the small nutrient arteries. In the early 
stages, with adequate hypertrophy, symptoms may be wanting, 
though a strong action of the heart and an increase in its size may 
be detected. Later, progressively increasing weakness of the cir- 
culation develops, and eventually all the signs of cardiac failure, 
just as in advanced valvular disease. Irregularity of the heart's 
action is much more pronounced than in valvular disease, and is 
particularly prominent when the walls of the auricles are especially 
involved. It has been ascribed to implication of the intracardiac 
mechanism. No satisfactory demonstrations have, however, been 
made, and for the present it can only be said that the irregularity 
of action results from the disease of the muscle and the conse- 
quent disturbance of its automatic contractility. 

Angina Pectoris. — In many cases of fibroid heart, paroxysms 
of pain occur. These may be moderate in severity and without 
definite characters, or they may be severe and of a uniform kind. 
The latter constitute the condition called angina pectoris. This is 
especially marked and frequent in cases of fibroid heart associated 
with advanced sclerosis of the coronary arteries. The cause of 
the paroxysm is uncertain. It may be the result of occlusions by 
embolism or thrombosis of branches of the coronary arteries. It is 
certainly in many cases associated with strain of the heart-muscle 
in its efforts to propel the blood. Neither of these explanations 
suffices for all cases. Changes in the intracardiac ganglia and in 
the fibers of different parts of the cardiac nervous mechanism 
have been described, but are of uncertain significance. 

Deterioration of the general health associated with fibroid 
heart may be the direct result of failing circulation, but may also 
result from associated widespread arteriosclerosis. The latter 
mode of operation is perhaps the more frequent. 

HYPOPLASIA AND ATROPHY. 

Hypoplasia of the heart is a congenital condition in which 
the heart is insufficiently developed and remains undersized 

25 



386 



TEXT-BOOK OF PATHOLOGY. 



throughout life. This condition is frequently associated with 
hypoplasia of the aorta and other large vessels, and sometimes 
with a similar condition of the generative organs. Persons hav- 
ing a predisposition to tuberculosis and women who develop 
chlorosis not rarely present the conditions referred to. These in- 
dividuals are often of delicate structure, with feeble or unstable 
circulation, and, in the case of males, of effeminate nature and 
appearance. The heart is small in size, and, as a rule, uniformly 
affected in all parts. The epicarclium may be somewhat wrinkled, 
and this condition, no doubt, has often led to the description of 
cases of this sort as instances of atrophy. Many cases of 
supposed hypoplasia are doubtless instances of true atrophy, 
the size of the heart being strictly proportioned to the emaciated 
body. 

Atrophy of the heart is usually described as occurring in 
two varieties, simple and brown atrophy. It is very doubtful, how- 
ever, if simple atrophy ever occurs. Many of the cases so desig- 
nated were doubtless hypoplasia, and other cases probably brown 
atrophies. 

Etiology. — Atrophy of the heart usually occurs in persons of 
advanced age ; but is occasionally met with in the young. It 

results from simple senility, or from 
various cachectic or wasting diseases, 
such as tuberculosis, carcinoma, and 
the like. 

Pathologic Anatomy. — The heart 
is small in size, sometimes weighing 
but a third or fourth of its normal 
weight. The capsule, or epicardium, 
is wrinkled, and may be somewhat 
thickened by fibrous-tissue over- 
growth or by fatty or mucoid change 



| 



Fig. 172.— Atrophy of the heart, Fig. 173.— Brown atrophy ol 

seen from the front (two-thirds the heart-muscle, 

natural size) (Bramwell). 

The vessels are conspicuously tortuous (Fig. 172). The muscle is 
flabby and often quite dark in color. 




f 



DISEASES OF THE CIRCULATORY SYSTEM. 387 

Microscopically the fibers are found smaller than normal, and 
contain excess of pigment. The latter is brownish or black, and 
at first situated at the poles of the muscle-nuclei (Fig. 173). Later 
the whole fiber may be uniformly pigmented. Sometimes the mus- 
cle-fiber is converted into a hollow sheath, containing scattered 
pigment-granules and more or less fragmented nuclei. Complete 
destruction of the fiber may lead to the apparent occurrence of 
pigment between the muscle-fibers. The pigment does not con- 
tain iron, and seems to be a derivative of the albuminous con- 
stituents of the fibers. 

Localized atrophy of the fibers may occur around areas of 
disease of the heart-muscle, such as foci of myocarditis, tubercles, 
gummata, etc. The fibers present the same appearances as those 
just described. 

Pathologic Physiology. — Atrophy of the heart-muscle does not 
often occasion striking results or symptoms, as the process is in 
most cases commensurate with the general emaciation and de- 
creased demand. Occasionally irregular action of the heart is 
noted, and sudden death has sometimes occurred. 

HYPERTROPHY AND DILATATION. 

Hypertrophy and dilatation are usually associated and result from 
the same causes, the degree of hypertrophy or of dilatation present 
in a given case depending upon the suddenness of action or the 
intensity of the cause, and upon the state of the heart itself. A 
sudden strain may cause immediate dilatation ; repeated strains of 
less severity cause hypertrophy in a well-nourished heart, or in- 
creasing dilatation in one the seat of myocardial weakness or 
degeneration. 

• Etiology. — The influence of valvular diseases (q. v.) of the heart 
in developing hypertrophy has been sufficiently discussed. Vari- 
ous other causes may lead to overwork or cardiac strain, and occa- 
sion hypertrophy or dilatation. We may classify the causes 
in accordance with their operation upon either or upon both 
ventricles. 

Causes Acting- on the Left Ventricle. — All forms of arterial 
disease, but especially diffuse arteriosclerosis, increase the work of 
the left ventricle notably, and may cause marked changes in it, 
Aneurysms of the aorta, however, have surprisingly little effect. 
Chronic Bright' s disease, especially the interstitial form, is a well- 
known cause. It probably acts in several ways : partly by the 
associated arterial disease, partly by vascular contraction due to 
toxic products, and partly by the direct stimulation of cardiac 
action by the same causes. Excessive exercise or laborious occu- 
pations (mining, blacksmithing, etc.) may act upon the whole 
heart, but especially upon the left ventricle. 



388 



TEXT-BOOK OF PATHOLOGY. 



Causes Acting* on the Right Ventricle. — Diseases of the 
lungs and pleura, such as emphysema, fibroid phthisis, and pleural 
synechia?, are frequent causes of hypertrophy and dilatation of the 
right ventricle. 

Causes Acting on the Heart as a Whole. — General func- 
tional overstimulation may cause uniform enlargement of the 
organ. This may be seen in cases of hysteria, exophthalmic 
goiter, and other diseases in which the overaction is due to ner- 
vous influences. Excessive eating and drinking affect the left more 
than the right ventricle, but influence both sides to some extent. 
Habitual, excessive beer-drinking is most striking in its effects, 
and doubtless acts through the constantly recurring overdistention 
of the blood-vessels, as well as through the excess of nutriment 
and direct stimulus conveyed to the organ. Pericardial adhesions 
may occasion continuous overaction of both ventricles. 

Any of the causes named may occasion hypertrophy or dilata- 
tion, or both. The degree of hypertrophy is dependent upon the 
previous integrity of the heart-muscle, the state of the general 
health, and the manner of action of the cause. Sudden strains 
are more likely to cause dilatation, and pure dilatation may result 
if the muscle of the heart is degenerated. This is illustrated by 
cases of acute dilatation of the heart in the course of infectious 
fevers. 

Pathologic Anatomy. — Four forms of enlargement of the heart 
may be distinguished. First, the walls are thickened, and the 
cavities are smaller than normal ; this is known as concentric 
hypertrophy, but it is likely that the decreased size of the cavities 
is due to post-mortem contraction ; second, hypertrophy of the 
walls with normal cavities is spoken of as simple hypertrophy ; 
third, hypertrophy with cavities of increased size is known as 
eccentric hypertrophy , or hypertrophy with dilatation; and, fourth, 
there may be pure dilcdcdion without hypertrophy. In hyper- 
trophy the muscle-substance is darker than normal and is increased 
in consistency. Microscopically the fibers are increased in thick- 
ness, and there is probably also increase in the number of the 
fibers. The nuclei of the muscle are swollen and multiply ; myo- 
cardial degeneration (fibro-fatty) is often associated. When dila- 
tation is present the heart-muscle is usually softer, more flabby, 
and generally somewhat lighter in color, due to associated degen- 
eration. 

The shape of the heart varies from the normal. When the 
left ventricle is hypertrophied the organ is increased in length 
and extends further to the left than normal (Fig. 174). When 
the right ventricle is hypertrophied the organ assumes a rounded 
shape ; its apex is less sharp, and the transverse measurement of 
the organ is greatly increased. The weight and size of the heart 
may increase enormously, and the term cor bovinum is often highly 



DISEASES OF THE CIRCULATORY SYSTEM. 



389 



appropriate. Weights of from 500 to 800 g. are not infrequent, 
and may be greatly exceeded. Stokes recorded a case in which 
the weight was 1980 g. 

Pathologic Physiology and Results. — Hypertrophy is a rel- 
ative process which serves to counterbalance the valvular or 




Fig. 174.— Hypertrophy of the left ventricle (Ziegler). 



other impediments to the circulation. Occasionally there may be 
excessive hypertrophy, but, as a rule, it is merely sufficient to 
maintain the circulation under ordinary conditions with less re- 
serve power than is met with in health. In consequence valvular 
lesions or arteriosclerosis may occasion no symptoms for a long 
time, provided the individual leads a quiet life. Eventually, 
however, when intercurrent diseases have determined cardiac 
weakness, or when the impediment to the circulation has grown 
progressively to an excessive degree, dilatation ensues and fail- 
ure of the circulation is the consequence. When the left ventri- 
cle is at fault congestion of the pulmonary system occurs, and 
edema, hemorrhage from the lungs, or thrombosis with infarction 
of the lungs may take place. When the right ventricle fails 
general systemic congestion, cyanosis, and dropsy are the conse- 
quence. 

Great hypertrophy, while it results from arterial disease, very 
frequently reacts upon the arteries and increases existing arterial 
disease, or occasions arterial disease when it has not previously 
existed. This is due to the increased force with which the blood 
is projected from the ventricular cavity and the increased dis- 
tention which the arteries suffer in consequence. 



390 



TEXT-BOOK OF PATHOLOGY. 



ANEURYSM. 

Aneurysm of the heart is a rare condition. It is usually found 
in the anterior wall of the left ventricle, near the apex, but may 
affect any part of the auricles or ventricles. Sometimes it is dim- 




Fig. 175.— Aneurysms of the left ventricle : the sac through which the probe was passed 
was situated posteriorly; the unopened aneurysm on the right was anterior; the heart 
is somewhat twisted out of its usual shape to show both sacs in the illustration (Sailer). 

cult to distinguish simple dilatation from aneurysm. The usual 
cause of aneurysm is coronary obstruction, with resulting degen- 
eration of localized areas of the wall of the heart. First, there is 
softening (myomalacia), and this may occasion acute aneurysmal 
dilatation and even rupture of the heart. In other cases the 
degenerated area becomes fibrous and subsequently dilates. Acute 
aneurysm of the heart-wall may similarly occur in cases of mural 
endocarditis. Rupture in such chronic cases is a rare termination. 

WOUNDS AND RUPTURE OF THE HEART. 

Non-penetrating and even penetrating wounds of the heart- 
wall are sometimes recovered from, the injury being repaired by 
scar-tissue or fibrous myocarditis. As a rule, penetrating injuries 
occasion rapid death by hemorrhage into the pericardium. Spon- 
taneous rupture of the heart may be occasionally the result of 



DISEASES OF THE CIRCULATORY SYSTEM. 391 



severe strain of a normal heart, but, as a rule, it occurs when 
there is myocardial disease. Myomalacia cordis, fatty degenera- 
tion, malignant endocarditis, and abscess are the conditions most 
likely to occasion rupture. 

INFECTIOUS DISEASES. 

Tuberculosis may occur in the form of acute miliary tuber- 
culosis, affecting either the endocardium, myocardium, or peri- 
cardium ; while caseous tubercles result from extension of tuber- 
cular adenitis from the anterior or middle mediastinum. 

Syphilis is rare, but may occur in the form of gumma or of 
diffuse infiltration. Gummata may lie immediately beneath the 
pericardium or endocardium, and after softening by degeneration 
may rupture on the surface. 

Actinomycosis may involve the heart by extension from the 
mediastinum or by embolism. White or grayish nodules are 
formed, and subsequently degenerate. 

NEW GROWTHS AND PARASITES. 

Primary tumors of the heart are extremely rare. Sarcoma, 
fibroma, lipoma, myxoma, and myoma have been met with, and 
usually occur in the form of wart-like growths projecting into the 
cavities beneath the endocardium. Organized pediculated thrombi 
have frequently been mistaken for tumors. 

Secondary tumors are more common. Sarcomata of the 
mediastinum may involve the pericardium, or even the heart-wall, 
by direct extension, while secondary carcinomata and sarcomata 
may affect the myocardium by metastasis. In the latter instances 
nodular formations are seen embedded in the heart-muscle. 

Parasites. — Echinococcus cysts are occasionally seen beneath 
the endocardium or pericardium, and may rupture into the cavities 
of the heart, with resulting embolism. The cysticerci of Taenia 
solium and of Taenia saginata have occurred in man, but are more 
common in animals. The larval Pentastomum denticulatum is a 
rare parasite of the heart. 

THE PERICARDIUM. 

The pericardium is a membranous sac enclosing the heart and 
the root of the great blood-vessels. It is composed of a fibrous 
outer layer, and is lined within by flat endothelial cells. Normally 
it contains from 5 to 50 cc. of clear serous liquid. 

Partial or complete absence of the pericardium is sometimes 
seen, especially in cases of ectopia of the heart. Occasionally 
diverticula are present congenitally. 



392 



TEXT-BOOK OF PATHOLOGY. 



CIRCULATORY DISTURBANCES. 

Hyperemia of the pericardium may occur in valvular heart- 
disease or in cases of tumor or aneurysm causing intrathoracic 
pressure. 

Hemorrhages. — Extreme passive congestion with ecchy- 
motic hemorrhages is found post-mortem in cases of death from 
asphyxia. Small punctate hemorrhages are also occasioned by 
various infectious diseases and by certain poisons, as phosphorus. 
They are also seen in pernicious anemia, scurvy, purpura, and 
other blood diseases. 

Hemopericarditim is a term applied to accumulation of 
blood in the pericardial sac. It may result from rupture of the 
heart or of aneurysms of the aorta, pulmonary artery, or coronary 
arteries. The serous effusion of inflammatory conditions of the 
pericardium may sometimes contain considerable blood which has 
escaped from the small blood-vessels in the inflammatory tissue. 
This is more common in inflammatory effusions of the pericardium 
than of other serous membranes, and is particularly true of tuber- 
culous and cancerous cases. 

Hydropericardium, or dropsy of the pericardium, may occur 
when passive congestion is continued, or as a part of a general 
anasarca. Occasionally the liquid is milky {chylous hydroperi- 
cardium). 

INFLAMMATION. 

Inflammation of the pericardium, or pericarditis, is 

the most important pathologic process affecting this part of the 
body. 

Etiology. — Pericardial inflammations may be primary or sec- 
ondary. In the former the irritants are conveyed to the pericar- 
dium through the blood, while in the latter the inflammation 
results from extension. Primary pericarditis occurs in association 
with various infectious diseases, notably acute rheumatism, scarlet 
fever, small-pox, influenza, and intense septic infections. It is 
also met with in the course of nephritis, either acute or chronic. 
Secondary pericarditis may result from extension of inflammation 
from the pleura, the lung, the mediastinal glands, the sternum, the 
esophagus, and stomach, or from the heart itself. 

In many instances, even where the pericarditis has occurred in 
the course of an infectious disease, micro-organisms are not dis- 
covered in the exudate ; this may be due to the arrest of the 
micro-organisms in the pericardial tissues ; staphylococci, strepto- 
cocci, pneumococci, and tubercle-bacilli have all been found. 

Pathologic Anatomy. — Several varieties may be distinguished, 
though one form may merge into another. 

Fibrinous or Dry Pericarditis. — The first change noted in 



DISEASES OF THE CIRCULATORY SYSTEM. 



393 



pericarditis is a dulness or lusterless condition of the surface of 
the membrane. Somewhat later distinct granulations, or a thin 
coating of fibrin, appear upon the surface, and this may increase 
until the deposit has a notable thickness. The movements of the 
heart may give the latter a marked roughness or rugosity, and the 
term applied by older writers, cor villosum, is not inappropriate 




Fig. 176.— Acute pericarditis (Bramwell). 



(Fig. 176). Microscopically there is seen a deposit of granular or 
fibrillar fibrin upon the surface, whilst the endothelial cells are 
loosened and partly degenerated, and the subendothelial tissues 
are infiltrated with round cells. The blood-vessels are generally 
widely dilated, and punctiform hemorrhages may be observed. 

Serofibrinous Pericarditis. — The pericardial exudate rarely 
remains purely fibrinous in character. Usually there is seen some 
serous outpouring, and the sac becomes distended with more or 



394 



TEXT-BOOK OF PATHOLOGY. 



less abundant turbid, serous liquid, in which flakes of fibrin are 
suspended. In such cases the fibrinous deposit is generally slight. 
Later the fluid may be reabsorbed, leaving a simple fibrinous 
pericarditis. 

Purulent pericarditis, or pyopericardium, may begin as a 
fibrinous or serofibrinous process, or it may assume the suppura- 
tive form from the very start. In these cases the cause of the 
pericarditis is usually some intense general infection, as in puer- 
peral pyemia and septicemia, or it may be a local infection, as in 
cases in which an esophageal or gastric ulceration has ruptured 
into the pericardium, or in which a caseous tubercular focus or 
purulent pleurisy has found a similar discharge. The pericardial 
sac is filled with more or less purulent or seropurulent liquid, and 
the pericardium itself is covered with fibrinopurulent exudate. 
The superficial layers of the myocardium are frequently involved 
by inflammatory edema, myocarditis, or fatty degeneration. 

Hemorrhagic pericarditis is met with in individuals of low 
vitality and in persons suffering from scurvy, purpura, and similar 
affections. Pericarditis accompanying tuberculosis or cancer of 
the pericardium is specially prone to assume a hemorrhagic type. 
Usually the exudate is serous, but distinctly colored with blood ; 
sometimes it is almost completely hemorrhagic. 

Terminations of Acute Pericarditis. — Any of the forms described 
may persist for a considerable length of time without change, but 
usually certain alterations are noted. In the fibrinous variety, or 
in the serofibrinous form, after the liquid has been reabsorbed, the 
visceral and the parietal pericardium lie in contact and are aggluti- 
nated by the exudate. Gradually the inflammatory processes 
beneath the fibrinous exudate extend into the fibrinous coating ; 
connective-tissue hyperplasia and new formation of blood-vessels 
follow, and granulation-tissue unites the adjacent layers of pericar- 
dium. At the same time the fibrinous exudate is reabsorbed and 
subsequently organization of the granulation-tissues is completed. 
Fibrous adhesions binding the two layers of the pericardium 
together ensue, and at times complete obliteration of the sac is the 
consequence (Figs. 177 and 178). In cases in which the inflam- 
mation is slight, or in which the layers are kept apart by persist- 
ent serous exudate, the areas of inflammation gradually become 
thickened by new-formed fibrous tissue, and there remain upon 
the surface of the pericardium sclerotic spots, often spoken of as 
" milk spots." Occasionally portions of the fibrinous exudate re- 
main unabsorbed, and together with the thickened membrane 
itself and the adhesions suffer calcareous infiltration. The 
heart may thus be encased in calcareous plates of considerable 
thickness. 

Purulent pericarditis may terminate by discharge of the exu- 
date into the esophagus, stomach, pleura, or even into the bronchi, 



DISEASES OF THE CIRCULATORY SYSTEM. 



395 



and by the subsequent adhesion of the two layers of the sac. In 
other cases gradual inspissation of the pus takes place and the 
cheesy residue may remain or eventually become calcareous. 




Fig. 177.— Adhesive pericarditis, showing fibrin-deposit, with new blood-vessels extending 
upward into it (Perls). 

Associated Conditions. — While, on the one hand, pericarditis 
often follows inflammatory processes in the surrounding parts, it, 




Fig. 178.— New blood-vessels and fibroblastic cells in a beginning adhesion of the 
pericardial layers. 

on the other hand, not infrequently occasions disease of the adja- 
cent structures. In most cases of severe acute pericarditis there 



396 



TEXT-BOOK OF PATHOLOGY. 



is some associated inflammation of the mediastinal structures and 
of the pleura contiguous to the pericardium. Cases which termi- 
nate with the formation of fibrous adhesions within the pericardial 
sac usually present, also, mediastinal and pleural adhesions with 
the external surface of the pericardium (pericarditis interna et 
externa). Myocarditis extending to a depth of 1 or 2 mm. is seen 
in nearly every case of pericarditis. In cases in which considerable 
pericardial exudate is present the heart-muscle is pressed upon and 
impeded in function, so that venous congestions are commonly 
observed. Adhesive pericarditis leads to hypertrophy and, later, 
dilatation of the chambers of the heart. 

INFECTIOUS DISEASES. 

Tuberculosis of the pericardium may result from the exten- 
sion of pulmonary or pleural tuberculosis, or of tubercular affec- 
tions of the mediastinal glands. More rarely direct infection may 
occur through the medium of the circulation. Miliary tubercles 
are formed in the subserous and serous layers of the membrane, 
while the surface is covered with fibrinous exudation. The attend- 
ant pericarditis may be entirely fibrinous and the tubercles may 
be hidden from view by a thick deposit. In other cases there is 
serous or hemorrhagic or purulent exudation, the latter especially 
in cases in which caseous vomicae have ruptured into the pericar- 
dial sac. Tuberculous pericarditis may terminate by gradual ab- 
sorption of the exudate and fibrous adhesion, sometimes with 
calcareous infiltration. In other cases the necrotic and destructive 
changes characteristic of tuberculous processes elsewhere gain the 
ascendency, and the disease proves fatal by the seriousness of the 
cardiac involvement. 

Syphilis is an extremely rare condition. Certain indurative 
changes in the pericardium have, however, been met with in asso- 
ciation with syphilis of the heart. 

Actinomycosis may result from extension of actinomycosis 
of the mediastinum or of the lungs. 

TUMORS AND PARASITES. 

Primary tumors, such as lipoma and fibroma, are extremely 
rare. Secondary carcinoma and sarcoma are more frequent. 
They result from similar growths in neighboring structures. 
Hydatid cysts and cysticerci are occasionally met with. 

PNEUMOPERICARDIUM. 

Pneumopericardium (air in the pericardium) may result from 
perforation of the sac in cases of fracture of the ribs or from pene- 
tration of foreign bodies through the esophagus into the peri car- 



DISEASES OF THE CIRCULATORY SYSTEM. 397 



ilium. It also results from rupture of gastric or esophageal ulcers, 
and a certain amount of gaseous accumulation complicates purulent 
pericarditis when the exudate undergoes decomposition. The 
association of air and pus (pneumopyopericardium) more often 
results from secondary purulent inflammation after the develop- 
ment of pneumopericardium. 

THE ARTERIES. 

Anatomic Considerations. — The arteries and veins consist 
of three coats, called, respectively, the intima, or inner coat, the 
media, or middle coat, and the adventitia, or external coat. The 
intima consists of a layer of endothelial lining-cells, below which 
there is a thick fibrous layer and then an elastic membrane. The 
middle coat consists of smooth muscle-fibers, while the outer coat 
is composed of the fibro-elastic tissue. Small blood-vessels, the 
vasa vasorum, ramify through the adventitia and media, but the 
intima is avascular. 

CONGENITAL DEFECTS. 

Certain defects of distribution and of origin of the larger 
trunks have been referred to in the discussion of congenital defects 
of the heart. Very commonly there are anomalies in the arrange- 
ment of the peripheral branches, but these are of merely anatom- 
ical interest. 

Hypoplasia. — A condition of importance is congenital small- 
ness, or hypoplasia. This may affect the aorta and larger vessels 
together with the heart, or it may be confined to the blood-vessels, 
the heart being normal. Vascular hypoplasia has been especially 
met with in chlorotic girls, and also occurs in persons of tubercu- 
lous habit. The aorta is sometimes so small that it barely admits 
the little finger, and the walls are usually correspondingly decreased 
in thickness. Decided elasticity of the coats of the vessels may 
be observed. 

HYPERTROPHY. 

This occurs when a collateral circulation is established in con- 
sequence of obstruction of an artery. Similarly in the new for- 
mation of tissue the blood-vessels first formed are delicate vascu- 
lar channels, which subsequently hypertrophy and are converted 
into well-developed arterioles. In this case there is a uniform 
overgrowth of each of the component parts of the blood-vessel, 
and not a mere hyperplasia of one or another coat. 

ATROPHY. 

Atrophy may occur in a part which is undergoing general 
atrophy, or in consequence of pressure and anemia of certain 



398 



TEXT-BOOK OF PATHOLOGY. 



areas. Degeneration of the walls usually takes place in such 
cases, and the conditions are therefore more properly considered 
among degenerations. 

DEGENERATIONS. 

Fatty Degeneration. — Any one of the coats may be affected, 
but the process is most common in the intima. Fatty degenera- 
tion is one of the important factors in atheroma ; more rarely it 
occurs as an independent affection of the blood-vessels. In the 
latter case disturbances of circulation and toxic agencies in the 
blood are the immediate causes. Small white or yellowish spots 
or streaks may be seen in the endothelium, and microscopically 
the endothelial cells may be found granular or filled with oil- 
drops. In cases of greater severity there may be actual erosion 
of the endothelial surface. In cases in which the media is affected 
the muscle-cells undergo fatty degeneration. Fatty degeneration 
may occasion rupture of the blood-vessels, or calcareous infiltra- 
tion may ensue. 

Calcareous infiltration is the common termination of athe- 
roma, but sometimes calcification of the intima or media, or even 
of the entire wall of the vessel, may be observed without arterio- 
sclerosis. The process is most common in the intima and media, 
and, aside from the instances in which it is a part of atheroma, it 
may occur in consequence of circulatory disturbances, or as the 
result of bone-disease, with destruction of osseous tissue and sur- 
charge of the blood with earthy salts. 

Hyaline degeneration is a condition, the nature and uniform 
character of which remain in doubt. A form of hyaline degenera- 
tion is very common in the hyperplastic tissue of arteriosclerosis, 
and is generally the first evidence of beginning degeneration. It 
is met with in small blood-vessels which are obstructed by thrombi, 
or which are subjected to destructive pressure by inflammatory 
new growths or other causes. Not infrequently it is due to infec- 
tious fevers or intoxications, and in these cases the small arteries 
and the capillaries are prone to be affected. Hyaline degeneration 
of the blood-vessels is the striking feature of certain cylindromata 
(see Fig. 54). The artery may show a uniform or a more nodular 
glass-like thickening, and under the microscope the subendothelial 
tissue or the adventitia, or the entire wall of the blood-vessel may 
be found converted into vitreous substance. Rupture of the 
affected vessel is a not infrequent result. 

Amyloid degeneration commonly begins in the blood-ves- 
sels of the parts of the body in which this disease is found. In the 
kidneys the capillary tufts of the Malpighian bodies and in the 
spleen the capillaries within the lymphoid nodes are first affected. 
In these cases the entire wall of the vessel is involved, and pre- 



DISEASES OF THE CIRCULATORY SYSTEM. 399 



•sents the characteristic appearances of the disease. Amyloid disease 
is sometimes found in the intima of the larger blood-vessels, occur- 
ring in small linear or punctate areas, and scarcely to be recog- 
nized excepting by chemical tests. 

INFLAMMATION. 

Inflammation of the arteries may affect the inner, the middle, 
or the outer coat, and in a strict anatomical sense the terms 
endarteritis, mesarteritis, and peri -arteritis are justified; but, as a 
rule, all three coats are more or less involved at the same time, 
and no practical distinction can be drawn. There may be acute 
or chronic inflammation. 

Acute Arteritis. 

Acute arteritis may be of two kinds : a suppurative, or necrotic, 
form, and a productive form. 

Acute suppurative arteritis occurs in the arteries travers- 
ing areas of suppurative inflammation, and results from the exten- 
sion of the suppurative process. It may also occur in consequence 
of the lodgement of infected emboli or as a result of infection of 
thrombi within the vessels. 

When the process extends from without, the adventitia and 
then the media are infiltrated with round cells, and in cases of 
some of the larger vessels there may be visible points or collec- 
tions of pus. The process may extend as deeply as the intima, 
and may completely perforate the wall of the vessel, leading to 
hemorrhage. The intima itself is not directly involved by the 
suppurative process from the lack of independent blood-supply, 
but the emigrated leukocytes may infiltrate it, and degenerative 
changes are common in the endothelium. Where the process 
begins by infection within, as through softened thrombi or infectious 
emboli, there is first necrotic or degenerative destruction of the 
intima, and subsequently infiltration of the media and adventitia 
with emigrated round cells. 

A form of infectious arteritis resembling malignant endocarditis 
has been observed in association with that condition in a few 
instances. Ulcerated patches are seen in the intima of the aorta, 
and acute aneurysmal dilatation or even perforation has been met 
with. 

Acute productive arteritis is most commonly the result 
of tissue-changes surrounding the arteries, and is therefore con- 
stantly met with in diseases of organs leading to overgrowth 
of connective tissue. The condition is chronic rather than acute 
in such instances. Acute productive arteritis occurs as a conse- 
quence of thrombosis within the blood-vessels when the latter are 



400 



TEXT-BOOK OF PATHOLOGY. 



not infected. The term thrombo-arteritis has been applied to these 
cases. It is by thrombo-arteritis that wounds of vessels are closed 
and the lumen of the blood-vessels at the point of ligation perma- 
nently obliterated. 

The changes affect mainly the intima and the adventitia, both 
of which coats are densely infiltrated with round cells. The 
thrombus, which was the original cause of the arteritis, or which 
has resulted from the arteritis, becomes similarly infiltrated with 
round cells, and as the process advances is found to be penetrated 
by fibroblastic cells, which probably take origin from proliferation 
of the endothelial-lining cells or from other connective-tissue cells 
in the walls of the vessels. New blood-vessels spring from the 
vasa vasorum and penetrate the thrombus, and a lesser number of 
new vessels may enter the thrombus directly from the lumen of 
the occluded vessel itself (see Fig. 7). The process of organization 
takes place as in the serous surfaces generally, and, as new connec- 
tive tissue is formed, the thrombus is gradually removed and the 
lumen of the vessel may become completely obliterated. Less ex- 
tensive involvement of the vessel may lead to the formation of 
bands of adhesion passing from one side of the vessel to the other, 
and causing considerable deformity and distortion. In other cases 
there may be merely thickening of the intima as a final result, the 
thrombus having been washed away or absorbed. The media 
usually takes very little part in the process, being merely infil- 
trated with round cells, but the entire wall of the vessel may 
become fibroid in the terminal stages and the separate coats may 
be indistinguishable. 

Peri-arteritis Nodosa. — Under this name has been described a form 
of productive inflammation of the adventitia leading to the formation of 
fibrous nodules. In some of these cases there is no doubt a different path- 
ology, as in the instances in which the intima has been found to protrude 
in a hernious manner through defects in the media, but in most cases the 
disease is a productive peri-arteritis (see also under Aneurysm). 

Arteriosclerosis. 

Arteriosclerosis, or endarteritis chronica deformans, 

is a chronic degenerative and inflammatory disease of the arterial 
system. It may be confined to the arteries, or may be more 
extensive, involving the capillaries as well, when the term arterio- 
capillary fibrosis (Gull and Sutton) is applicable. Sometimes the 
veins also are involved, and for this condition the name angio- 
sclerosis has been proposed. 

Etiology. — Arteriosclerosis is a physiologic process of old age, 
and probably begins as early as middle life in most persons. The 
earlier occurrence of the disease or the more extreme grades of its 
severity are dependent upon a variety of causes, among which cer- 
tain chronic intoxications, viz., syphilis, gout, chronic alcoholism, 



DISEASES OF THE CIRCULATORY SYSTEM. 401 



and chronic nephritis, are prominent. An important cause is 
muscular exertion, and it is not uncommon to find marked in- 
stances in persons whose life or occupation has subjected them to 
unusual muscular strain. Cachectic conditions of various kinds 
may play a part, as in cases of carcinoma, tuberculosis, or inani- 
tion ; and sometimes the chronic arterial disease follows after 
acute infections, such as rheumatism, scarlet fever, typhoid fever, 
and the like. 

Pathogenesis. — Not a little difference of opinion has existed in 
regard to the manner in which the recognized causes of arterio- 
sclerosis operate. At first it was generally maintained that the 
infectious and toxic agencies directly irritate the inner lining of 
the blood-vessels and produce inflammatory thickening. This 
view has, however, been quite generally abandoned, and it now 
seems established that degenerative changes and loss of elasticity 
in the vessel-wall are the result of the primitive causes, and that 
the hyperplastic processes in the intima and other parts of the 
arterial wall are the ultimate result. 

In cases of arteriosclerosis occurring in old age, for example, 
the first disturbance of the blood-vessel consists in the loss of 
elasticity in the muscularis and the overdilatation of the blood- 
vessels. Secondarily, in consequence of this loss of elasticity, 
there is a hyperplasia of the intima, which serves in some measure 
to contract the lumen of the vessels and thus restore the vascular 
channels to their normal condition. In cases of purely patho- 
logic arteriosclerosis similar functional weakness of the muscularis 
or more pronounced and demonstrable degenerative changes may 
be the primary conditions, which in the end lead to arteriosclerosis.. 
In all cases the direct effect of elevations of blood-pressure may 
play an important part, and in cases of muscular overwork or of 
hypertrophy of the heart the increased vascular tension may be the 
all-important cause. 

Pathologic Anatomy. — Arteriosclerosis may be a diffuse process, 
affecting more or less uniformly a large part of the arterial system, 
or it may be a circumscribed or nodular condition. In the latter 
instances, which are most common in the aorta and large vessels, 
there are seen on the inner lining of the vessel nodular elevations, 
varying in size from the merest points to that of a small coin. 
These are raised a millimeter or two above the surface, and in 
their earlier stages have a translucent grayish color ; they are 
covered with smooth, unaltered endothelium. Later, degenerative 
changes ensue and the nodule becomes dull white or yellowish in 
color, and finally calcification may render it extremely hard (athe- 
romatous plate). The focus may, on the other hand, soften com- 
pletely by degeneration and may discharge into the lumen of the 
vessel, leaving a necrotic, ulcerated patch (atheromatous ulcer). 
Calcareous change may now occur, and the surface may be covered 

26 



402 



TEXT-BOOK OF PATHOLOGY. 



with thrombotic fibrinous deposits. These circumscribed areas of 
arteriosclerosis may be few in number and widely separated. In 
such cases the openings into the coronary arteries and the other 
branches of the aorta are the favorite seats. In other cases the 
plates may be so numerous and thickly set that the aorta is com- 
pletely transformed. 

Diffuse arteriosclerosis is especially frequent in elderly per- 
sons, and is more common in the small vessels than in the aorta. 
Sometimes it is associated with the nodular form ; sometimes 
the nodular change is completely wanting. 

Microscopically the nodular elevations are found to consist of 
dense sclerotic tissue in which deeply staining cells of elongated 
character may be visible, the hyperplasia affecting the subendo- 
thelial part of the intima in the earliest stages (Fig. 179). Sub- 




Fig 179 —Transverse section of a cerebral vessel, in a case of endarteritis nodosa (Birch- 

Hirschfeld). 

sequently degeneration of the nodule becomes manifest. At first 
the intercellular material assumes a hyaline character and becomes 
glassy in appearance. The cells themselves may suffer fatty 
degeneration from pressure. Later the whole area undergoes 
myxomatous or more particularly fatty degeneration, and breaks 
down, forming a pultaceous detritus in which fat-drops and choles- 
terin-plates are prominent (Fig. 180). Eventually calcareous 
granules are deposited. 

Fatty degeneration and calcification may also be apparent in 
the media, and more or less hyperplastic connective-tissue over- 
growth may be seen in the adventitia. In cases of diffuse arterio- 
sclerosis the media, as a rule, is thickened by hypertrophy of the 
muscle-fibers as well as by sclerosis ; but in the nodular forms the 
media is usually distinctly thinner than normal. Koster pointed 
•out that round-cell infiltration surrounding the small branches of 



DISEASES OF THE CIRCULATORY SYSTEM. 



403 



the vasa vasorum in the media is the earliest change in some 
instances. Considerable round-cell infiltration may be seen in the 
deeper layers of the intima and in the media, and new formation 




Fig. 180.— Atheromatous degeneration of a cerebral artery (Karg and Schmorl). 

of blood-vessels may be quite pronounced. Such changes, how- 
ever, are not usual and not characteristic. 

Results. — In the smaller blood-vessels, particularly in those of 
the brain, the hyperplastic process in the intima may proceed to 
such a degree that the lumen of the vessels is almost completely 
obliterated (endarteritis obliterans). Complete obliteration may 
take place by direct union of the opposite walls of the vessel, or 
there may be first thrombosis, with subsequent organization of the 
thrombus. In the aorta and in some of its larger branches the 
loss of elasticity consequent upon the formation of fibrous tissue 
and subsequent degenerations leads to gradual dilatation of the 
blood-vessel walls, either in the form of diffuse ectasia or of local- 
ized aneurysmal sacs. Sometimes the degeneration of the dis- 
eased area occasions spontaneous rupture of the vessel. 

Portions of the thrombotic deposits upon the roughened lining 
of the vessels, or portions of the degenerative tissue itself, may be 
discharged into the circulation, and may be carried to the periph- 
eral parts as emboli. 

Changes in Other Organs. — Diffuse arteriosclerosis places an 
impediment upon the heart which leads to hypertrophy of its walls, 
and in particular of the walls of the left ventricle. 

When the process affects the small blood-vessels in the sub- 
stance of the various organs, degenerative changes due to anemia 
and reactive hyperplasia of connective tissue are common results. 



404 



TEXT-BOOK OF PATHOLOGY. 



Thus, in cases of sclerosis affecting the cerebral vessels, cerebral 
softening is commonly met with, while in cases in which the 
branches of the coronary or of the renal arteries are aifected, 
degeneration and fibroid changes are seen in the heart and kid- 
neys. 

INFECTIOUS DISEASES. 

Syphilis may involve the blood-vessels in a variety of ways. 
No doubt, syphilitic infection is the most potent cause in the pro- 
duction of arteriosclerosis, but more specific involvement of the 
vessels occurs. Thus in areas of syphilitic infiltration and indura- 
tion or adjoining gumma ta, the blood-vessels present noteworthy 
changes. The intima and the adventitia, but particularly the 
former, undergo great hyperplasia, and the lumen of the vessel 
may be almost obliterated. The changes are first noted in the 
intima, where large numbers of epithelioidal cells are formed, 
while, later, infiltration of round cells is observed. The adven- 
titia is similarly, but less extensively, aifected. There is no his- 
tologic or macroscopic feature by which the syphilitic nature of 
the disease can be positively asserted. 

Tuberculosis. — The arteries may become involved in areas 
of tuberculosis, though, as a rule, they prove resistant for a long 
time. Typical caseous degeneration may be seen in the walls 
of the blood-vessels, beginning in the adventitia and gradually 
advancing toward the interior. In the lungs these changes are 
not infrequently seen in the walls of tuberculous cavities, and 
as a result there may be small aneurysmal dilatations at the 
points where the wall of the vessel has become eroded and weak- 
ened. It is from such vessels that the severe hemorrhages of the 
late stages of phthisis take place. Sometimes the blood-vessels 
of the tuberculous area present productive change leading to 
great thickening of the adventitia and of the intima, and there 
may be considerable narrowing of the lumen of the vessel. This, 
however, is less common than the degenerative changes before 
alluded to. 

ANEURYSM. 

Definition. — By aneurysm is meant a more or less localized 
dilatation of the arterial walls. The term has, however, been 
applied also to collections of blood outside of an artery enclosed 
by an adventitious wall and consequent upon a rupture of the ves- 
sel. The name false or spurious aneurysm has been specially 
applied to such cases, while the term true aneurysm is reserved for 
such as conform to the first definition. It is preferable to confine 
the single word aneurysm to the latter. 

I^tiology. — Aneurysms are always due to some weakness of 
the walls of the blood-vessel and to the distending force of the 



DISEASES OF THE CIRCULATORY SYSTEM. 



405 




blood within. It is therefore most common to find the disease in 
persons beyond the age of forty or forty -five years, and particu- 
larly in those who have acquired arteriosclerosis. Among the 
remote causes, therefore, are the causes of arterial disease — syph- 
ilis, gout, alcoholism, lead-poisoning, and other chronic intoxica- 
tions. Sometimes it would seem that there is an hereditary weak- 
ness of the arterial coats, and instances of aneurysm occurring in 
successive generations have been recorded. Even congenital aneur- 
ysms have been observed. As contributing causes may be ranked 
all conditions which increase the blood-pressure. Thus laborious 
occupations, hypertrophy of the heart, and diseases which occasion 
constant excess of blood-pressure give rise to arterial degeneration 
and also to dilatation of the vessel in a purely mechanical way. 
Sudden aneurysmal dilatation of the weakened vessel may occur 
after severe straining efforts, as in coughing, during labor, in the 
straining of obstinate constipation, etc. Of all the causes, syphilis 
is most important. 

More acute degenerative changes in the blood-vessels may lead 
to aneurysmal dilatations. Thus in the rare instances of acute 
aortitis in association with malig- 
nant endocarditis, small aneur- 
ysmal dilatations and even rupture 
of the aorta may occur. Embolism 
plays a part in a similar manner. 
Sometimes a calcareous embolus 
from a diseased valve of the heart, 
or from an atheromatous plate in 
the aorta, may lacerate the walls 
of the peripheral vessel, leading 
to the formation of a dilatation. 
In other cases infected emboli 
(as in malignant endocarditis or 
thrombosis with secondary de- 
generation of the clot) lodge in 
the peripheral vessels and occa- 
sion acute inflammatory or de- 
generative lesions of the walls, 
and eventually aneurysmal dila- 
tation. These cases are analogous 
to the aneurysms of lower animals, 
caused by animal parasites (Fig. 
181). 

The artery most commonly af- 
fected is the aorta, and in particular the thoracic portion. A 
majority of the aneurysms affecting the thoracic part of this 
vessel arise from the ascending limb, and not rarely it is one 
of the sinuses of Valsalva that first suffers dilatation. Next 




Fig. 181. 



Worm-aneurysm of the horse 
(Leuckart). 



406 



TEXT-BOOK OF PATHOLOGY. 



to the aorta in point of frequency, the popliteal, femoral, carotid, 
subclavian, innominate, axillary, and iliac vessels are affected. 



An interesting form, and one of great frequency and clinical signifi- 
cance, is that which affects the small blood-vessels of the brain, particularly 
the branches supplying the lenticu- 
lostriate body. This is the so-called 
miliary aneurysm, which is commonly 
the cause of cerebral hemorrhage 
(Fig. 182). It is simply a small 
saccular aneurysm due to weakening 
of the blood-vessel walls by sclerosis 
or degeneration. 

In some cases of the condition de- 
scribed as peri-arteriiis nodosa (see 
page 400) there has been discovered 
a hernious projection of the intima 
through defects of the media. These 
have been recorded as instances of 
congenital aneurysm ; but this expla- 
nation does not suffice for all cases 
(see Arteritis). 

In phthisical lungs there are often 
found somewhat similar hernious 
aneurysms, due to erosion of the ad- 
ventitia and media by the tubercu- 
lous process ; and it is from these that 
the severe hemorrhages of the late 
stages of phthisis occur. 





Fig. 182.— Miliary aneurysm of the brain. 



Fig. 183.— Cylindrical and some- 
what cirsoid aneurysm of the ab- 
dominal aorta ; an opening has been 
made to show the clot within (from 
a specimen in the Museum of the 
Philadelphia Hospital). 



Pathologic Anatomy. — Aneurysms may be of three kinds : 
(1) those in which there is quite general dilatation of all of the coats 
of the vessel, which therefore present themselves in the form 
of a more or less uniform dilatation (ectatic aneurysm) ; (2) those in 
which a local weakening leads to the formation of a saccular pouch, 
often communicating with the artery by a narrowed orifice (saccular 
aneurysm) ; and (3) those in which a rupture of the intima, and 
usually of portions of the media as well, has led to infiltration of 
blood between the tunics of the vessel-wall (dissecting aneurysm). 

1. Ectatic Aneurysm. — There is more or less uniform dilatation 
in these cases, and there may be distinguished fusiform or spindle- 



DISEASES OF THE CIRCULATORY SYSTEM. 407 



shaped and cylindrical varieties, according to the shape assumed 
(Fig. 183). In some instances the vessel is rendered tortuous by 
the unequal involvement of different portions, and to this form the 
term cirsoid aneurysm may be applied. The same term, as well as 
the name anastomotic aneurysm, is given to certain conditions of 
the arteries of the scalp and other parts which lead to the forma- 
tion of tortuous vessels standing out prominently beneath the skin ; 
but these are instances rather of hypertrophy of the coats, with 
increase of length and thickness of the walls, without in reality any 
aneurysmal dilatation at all. 

In ectatic aneurysms the intima and adventitia are usually 
thickened, and there are generally atheromatous patches in the 
former. The media is generally thinner than normal, and may be 
actually deficient in places. Ectatic aneurysms may show a cer- 
tain amount of thrombosis in the form of laminated clots, when 
there are pouchings or inequalities in the dilatation ; but very 
frequently there is no thrombosis. 

2. Saccular Aneurysm. — This is the most important variety. 
According to Thoma and others, the first step in the process is the 




Fig. 184.— Saccular aneurysm of the arch of the aorta, projecting forward and attached to 

the ribs (Ziegler). 

weakening or giving way of the media, followed by gradual dila- 
tation of the intima and adventitia. There results a saccular 
dilatation communicating with an artery, from which it arises by 
a more or less narrow orifice (Fig. 184). The aneurysmal sac 



408 



TEXT-BOOK OF PATHOLOGY. 



grows larger and larger, and may eventually rupture ; but even 
then a secondary retaining wall may be formed by condensation 
and reactive hyperplasia of the surrounding tissues. The wall of 
the aneurysmal sac consists of thickened adventitia and intima, the 
media being usually thinned and often completely wanting. The 
intima is generally covered with atheromatous plates, and the cav- 
ity, as a rule, contains more or less abundant laminated clots, 
which tend to contract and organize, or to suffer subsequent 




Fig. 185.— Saccular and partly ectatic aneurysm of the descending part of the arch of the 
aorta (from a specimen in the Museum of the Philadelphia Hospital). 

degeneration. The aneurysm, if small, may be completely healed 
by the organization of the clots within. 

The tissues surrounding the aneurysm are pushed aside or 
compressed, and may suffer extensive necrosis. In cases of 
aneurysm of the thoracic aorta the sternum and ribs may be 
eroded, and the aneurysm may project beneath the skin anteriorly 
and eventually rupture (Fig. 187). In other cases the trachea, 
bronchial tubes, or lungs are compressed, and rupture takes place 
through the trachea or bronchi (Fig. 188). In still others the sac 
projects posteriorly, erodes the bodies of the vertebra? and ribs, 
and may compress the spinal cord or may project beneath the 



DISEASES OF THE CIRCULATORY SYSTEM. 409 



tissues of the back. Occasionally communication is established 
with the large venous trunks, particularly the descending vena 
cava. Complete arrest or cure of an aneurysm may take place 
by organization of the clots contained, but such a result is rare. 

3. Dissecting-aneurysm is most common in the aorta. As the 
result of degenerative lesions or of mechanical injury, rupture of 
the intima occurs, and the blood finds its way between the coats 
of the artery, often burrowing to considerable distances. In a 
case under my observation the walls of the aorta were dissected 




Fig. 186.— Saccular aneurysm of the ascending part of the arch of the aorta (from a 
specimen in the Museum of the Philadelphia Hospital). 

as far as the bifurcation, where secondary ruptures had occurred 
in the intima (Fig. 189). Usually the dissection takes place in 
the media, which is thus separated into two parts. Subsequently 
the adventitious canal may become lined with endothelium, and 
in my case atheromatous plates had formed in the latter. 

Associated Conditions in Other Parts. — Some hypertrophy 
of the heart may occur when an aneurysm is situated near the root 
of the aorta, and particularly in instances in which direct press- 
ure is brought to bear upon the heart. As a rule, however, the 



410 



TEXT-BOOK OF PATHOLOGY. 



amount of hypertrophy is much less than might be expected. 
Pressure upon the venous channels is an early manifestation, and 




Fig. 187.— Aneurysm of the aorta : erosion of the sternum and projection of the sac 

beneath the skin. 

leads to passive congestion and often to dropsy and cyanosis. 
Necrosis of the parts which are directly compressed has already 




Fig. 188.— The trachea, showing perforation of an aneurysm of the aorta (from a specimen 
in the Museum of the Philadelphia Hospital). 

been alluded to. Portions of the clot within the aneurysmal 
cavity not rarely become separated, and are carried as emboli to 
the peripheral parts of the circulation. 



DISEASES OF THE CIRCULATORY SYSTEM. 411 



False or spurious aneurysms most commonly result from 
traumatism, though sometimes spontaneous rupture of the vessel is 
the immediate cause. The blood may find its way from the rupt- 
ured artery into the surrounding tissues, forming a blood-tumor, 
or hematoma, which becomes encapsulated by condensation of the 
surrounding tissues and by reactive overgrowth of connective 
tissue. The retaining wall thus formed may in some cases be 
lined with endothelial cells, and secondary inflammatory thicken- 
ing or atheromatous plates may form. When an artery and vein 




Fig. 189.— Dissecting-aneurysm of the aorta : the aneurysm began near the aortic 
valves and extended to the iliac branches, converting the aorta into a double tube: 
a, transverse, b, longitudinal section. 

are both injured, as is sometimes the case in phlebotomy, the blood 
may enter the vein and distend this markedly. The term aneur- 
ysmal varix is applied to such cases. In other instances the 
artery and vein communicate by an intermediate sac formed by 
the condensation of the intervening tissues, and for such the name 
varicose aneurysm is used. 

THE VEINS. 

Anatomical Considerations. — The veins resemble the 
arteries, excepting that the muscular coat is less well developed 
and that most of the veins are supplied with endothelial redupli- 
cations or folds, which act as valves and prevent the backward 
flow of the blood. 

CIRCULATORY DISTURBANCES. 

Thrombosis of the veins is the most important condition. 
This, however, is sufficiently considered under Thrombosis (p. 57). 



412 



TEXT-BOOK OF PATHOLOGY. 



DEGENERATIONS. 

Fatty degeneration of the intima and media may occur, as 
in the arteries, but it is comparatively rare and unimportant. 

Calcification is met with in veins which have become dilated 
or varicose, or otherwise diseased. 

INFLAMMATION, OR PHLEBITIS. 

Acute phlebitis is a comparatively common affection. It 
may occur as the result of inflammation, particularly infectious 
inflammation, in the neighborhood of the vein. In such cases the 
outer coat is first involved, and the term periphlebitis is properly 
applied. This condition is met with in association with infected 
wounds and phlegmonous inflammations of the subcutaneous 
tissues. The veins beneath the skin may be distinctly visible as 
blue streaks running in various directions. Microscopically there 
is found to be an invasion of the adventitia with round cells, and 
actual foci of suppuration are not uncommon. The cellular infil- 
tration may extend to the media and sometimes to the intima, and 
not rarely thrombosis occurs within. The thrombi thus formed 
may secondarily become infected, soften, and occasion septic embo- 
lism. 

In another group of cases phlebitis begins from within, and is 
the consequence of primary thrombosis of the vein (Figs. 1 90 and 
191). To such the name thrombophlebitis is applicable. The 




Fig. 190. — Thrombophlebitis of the femoral vein (from a specimen in the Museum of the 
Philadelphia Hospital). 

histologic changes are similar in these to those which occur in 
thrombo-arteritis, and as terminal results localized thickening of 
the venous wall or irregular contractions by the formation of 
fibrous adhesions and even complete obliteration of the venous 
channel may result. When the thrombus is thus organized or 
partially organized calcification may eventually occur, and in this 
manner phleboliths, or vein-stones, are formed. 

Chronic phlebitis, or phlebosclerosis, corresponds to 
chronic arteritis or arteriosclerosis. A certain amount of chronic 
inflammatory thickening of the vein ensues as a consequence of 
thrombophlebitis. Phlebosclerosis may also be due to overdis- 



DISEASES OF THE CIRCULATORY SYSTEM. 413 



tention of a vein resulting from thrombosis or other forms of 
obstruction, and thus plays a secondary part in dilatation of the 
veins, or phlebectasia. 

Phlebosclerosis may, however, occur as a widespread affection 
in association with arteriosclerosis, though rarely in equal degree, 
in consequence of certain systemic conditions — syphilis, alcohol, 
gout, etc. The changes occurring in the vein are practically the 




Fig. 191.— Phlebitis and periphlebitis of the umbilical vein of the new-born : purulent 
infiltration of the intima and adventitia; calcareous particles in the media (Birch- 
Hirschfeld). 

same as those in the artery, but the new-formed fibrous tissue in 
the intima less commonly undergoes degenerative changes and 
calcification than in arterial sclerosis. 

In cases of congenital syphilis an interesting form of thicken- 
ing of the intima, leading to stenosis or even complete obstruction, 
has been found in the veins of the umbilical cord, and less fre- 
quently in the portal vein. Similar hyperplastic endophlebitis has 
been found in the veins of the extremities in syphilis of adults. 

DILATATION OF THE VEINS ; PHLEBECTASIA ; VARICOSITY. 

Etiology. — Dilatation of the veins occurs from mechanical 
obstruction to the circulation or from weakness of their walls. 
It presents itself more commonly in dependent portions of the 



414 



TEXT-BOOK OF PATHOLOGY. 



body, and is particularly frequent in the veins of the legs, of 
the rectum, of the neck of the bladder, of the spermatic cord, 
of the scrotum, and of the vagina. 

Mechanical causes are most important. Thus in cases of 
cirrhosis of the liver, of obstinate constipation, and of pelvic 
tumors, dilatation of the veins of the rectum, causing hemor- 
rhoids, is frequent. In cases of abdominal tumors, repeated 
pregnancy, or other causes of obstruction to the venous return of 
the blood from the lower extremities, varicosity of the veins of 
the legs is frequently observed. Always, however, local disease 
of the veins themselves tends to make the dilatations more pro- 
nounced, and in addition systemic depression, and particularly 
cardiac weakness, are contributing causes which operate by aiding 
in the stagnation of the blood, which otherwise might pass by col- 
lateral channels to its proper destination. 

Pathologic Anatomy. — The veins in phlebectasia become 
dilated and also elongated, so that they soon assume a tortuous 
character. Not rarely masses of much-dilated veins lie closely 
aggregated in groups or clumps beneath the surface of the skin ; 
and communications may be established between the adjoining 
pouches of dilatation, and thus a cavernous tissue is formed. The 
walls of the dilated veins are usually considerably thickened 
(phlebosclerosis), and even calcification may occur in the intima. 

Results. — The circulation of the blood is slowed and throm- 
bosis is therefore frequent. The thrombi may undergo organiza- 
tion or calcification, or in other cases may soften and occasion 
embolism. When varicosities are established in the veins of any 
submucous tissue, catarrhal inflammation of the overlying mucosa 
is occasioned and generally proves obstinate. At the same time a 
certain amount of hyperplasia of the connective tissue between the 
dilated veins takes place and thickening of the mucous membrane 
results. When the subcutaneous veins are involved the skin is 
prone to become thickened and to present eczematous inflamma- 
tion, while the subcutaneous tissue may be greatly increased in 
thickness and density (phlebectatic elephantiasis, or pachydermia). 
Not rarely ulcerations of the skin of the lower extremity owe 
their origin to varicosity of the veins, and such ulcers are prone 
to prove indolent and obstinate. Hemorrhage may occur from 
varicosities of the submucous veins, particularly in case of hem- 
orrhoids and in the esophageal varicosities of drunkards. 

TUMORS. 

Tumors rarely begin in the walls of the veins, though myoma 
and sarcoma have been described. More commonly the walls of 
the veins are secondarily involved in cases of tumors surrounding 
them. 



DISEASES OF THE CIRCULATORY SYSTEM. 



415 



INFECTIOUS DISEASES. 

Tuberculosis not rarely attacks the veins, particularly those 
of the lungs. Perforation of the wall may take place, and miliary 
tuberculosis is a frequent consequence. 

Syphilis of the veins has already been referred to. 

THE LYMPHATIC CHANNELS. 

Anatomic Considerations. — The lymphatic system begins 
in the lymph-spaces, which are the spaces between the tissue- 
elements in all parts of the body. These lymph-spaces unite to 
form definite lymphatic capillaries, which are channels having 
w r alls composed of a single layer of endothelial cells. The lym- 
phatic capillaries unite to form larger vessels, and in these con- 
nective-tissue coats support the endothelial lining. 

INFLAMMATION. 

Inflammation of the lymphatic vessels, or lymphan- 
gitis, is always secondary to inflammatory affections of the parts 
surrounding the lymphatics, or of those parts from which the lym- 
phatics take their origin. In cases of infective lesions of the ex- 
tremities red lines, indicating the position and course of the inflamed 
lymphatics, may not infrequently be seen beneath the skin, extend- 
ing upward to the nearest lymphatic glands. Histologically the 
first change in such cases is swelling and ofttimes multiplication 
of the endothelial cells of the lymphatic vessel ; later, there may 
be accumulation of leukocytes within, and the lymphatic channel 
may be uniformly filled with pus or distended at different points. 
Usually a certain amount of perilymphangitis accompanies the 
process, and in cases of violent septic infection the surrounding 
tissues may become extensively involved in phlegmonous inflam- 
mation. Thrombosis may take place within the lymphatic chan- 
nel in cases of moderate severity, and obstruction ensue. The ter- 
mination is either in resolution or suppuration, with more or less 
widespread involvement of the surrounding tissues. Resolution 
may be only partial, the inflammatory changes going on to the 
formation of connective tissue, which may obliterate the channels, 
or the restitution of the wall of the lymphatic vessel may be im- 
perfect, and subsequent dilatation results. 

DILATATION OF THE LYMPHATICS, OR LYMPHANGIECTASIA. 

This condition may be an acquired or a congenital affection. 

Acquired dilatation of the lymphatics results from ob- 
struction to the larger channels, as in cases of pressure upon or 
thrombosis of the thoracic duct, or of obstruction of the lym- 



416 



TEXT-BOOK OF PATHOLOGY. 



phatic channels by filarise. In other cases it is due to inflamma- 
tions surrounding the lymphatics and leading to weakness of their 
walls. It is very commonly observed in the subcutaneous lym- 
phatics, and constitutes the endemic elephantiasis of warmer coun- 
tries. This condition is particularly common in the lower extrem- 
ities, scrotum, and labia, but may affect other parts. The skin is 
greatly thickened and the surface often of irregularly lobulated 
character. On incision into it there is found an abundant exuda- 
tion from the subcutaneous tissue of serous or of milky liquid. 

Obstructive dilatation of the intra-abdominal lymphatics is not 
unusual. Rupture of dilated branches in the genito-urinary tract 
may lead to chyluria. 

Congenital lymphangiectasia may take the form of a 
diffuse condition affecting the lymphatics more or less regularly 
in certain parts of the body, or it may appear in circumscribed 
areas, often in situations in which the ordinary lymphatic supply 
is not abundant. The diffuse form occasionally presents itself in 
the new-born in the form of edematous or semicystic swellings of 
the subcutaneous tissue, resembling those of elephantiasis. In the 
same group of cases belong the instances of congenital enlargement 
of the tongue (macroglossia) and of the lips (macrocheilia). In some 
of these instances the development of the condition does not occur 
until some time after birth, though the process is in reality con- 
genital. Localized lymphatic dilatations constitute the form of 
new growth known as lymphangioma (see General Pathology). 

INFECTIOUS DISEASES. 

Tuberculosis. — The lymphatics play an important part in 
the dissemination of tuberculosis within the organs, and they may 
themselves be involved in the disease. This is beautifully illus- 
trated in cases of intestinal tuberculosis with ulceration. In such 
cases the lymphatic channels in the serous coat may be seen radi- 
ating from a point opposite the ulceration toward the mesentery, 
and small miliary nodules are seen in their course. 

Syphilis. — The lymphatics may be involved in syphilitic proc- 
esses in their vicinity, but the changes are not characteristic. 

TUMORS. 

In addition to the lymphangiomata referred to, the lymphatic 
vessels are the primary seat of tumors resulting from multiplica- 
tion of the lining endothelial cells, which are known as endothelio- 
mata. These tumors are especially common in the serous surfaces, 
but may also be met with in the skin and elsewhere. The lym- 
phatics bear an important relation to the metastasis of malignant 
tumors, particularly of carcinomata. The carcinoma-cells enter 



DISEASES OF THE CIRCULATORY SYSTEM. 417 



the lymphatics and are carried by the stream to distant parts of 
the body ; sometimes the lymphatics near carcinomata are found 
densely packed with cancer-cells. 

PARASITES. 

The adult of the Filaria sanguinis hominis resides in the lym- 
phatic vessels, and the embryos may be present in large numbers 
(see General Pathology). 



THE THORACIC DUCT. 

Pathologic processes involving the thoracic duct resemble in 
general character those of the other lymphatic vessels, but the size 
of the duct and its anatomical relations make the diseases affect- 
ing it of somewhat greater significance than the same diseases when 
occurring in the smaller lymphatics. 

Thrombosis may occur in association with inflammation of 
the duct or without such, and there may be a permanent occlusion 
in consequence. Dilatation of the lower parts of the duct, as 
well as of the lymphatic vessels of the abdomen, may ensue, and 
sometimes the receptaculum or other portions of the duct may 
become cystic. Chylous ascites may likewise result. More com- 
monly collateral circulation re-establishes circulation and serious 
consequences are not observed. 

Dilatation of the thoracic duct may also result directly 
from cardiac failure with engorgement of the greater veins. The 
outflow of lymph is impeded, and in some cases the backward 
pressure of the blood through the superior cava may fill and dis- 
tend the upper part of the thoracic duct with blood. 

Inflammation occurs in consequence of various inflammatory 
diseases of the abdomen or of the pelvis, by the invasion of irri- 
tants through the lymph received from the affected areas. There 
may also be direct extension of inflammation in cases of abdominal 
disease, or in pleurisy or other intrathoracic affections. 

Tuberculosis affecting the abdominal portion of the duct is 
sometimes observed in cases of intestinal or mesenteric tubercu- 
losis, and may occasion secondary miliary tuberculosis, particu- 
larly the form in which the disease is subacute or chronic in its 
course (Weigert). 

Tumors. — Primary tumors are sometimes observed, and sec- 
ondary carcinoma is more commonly met with. 



27 



418 



TEXT-BOOK OF PATHOLOGY. 



CHAPTER IV. 
DISEASES OF THE RESPIRATORY SYSTEM. 

THE NASAL CAVITIES. 

Anatomic Considerations. — The mucous membrane of the 
nose is unusually prominent, especially over the lower turbi- 
nated bone, where it is 4 mm. thick. In the lower, or respiratory, 
parts of the nose the epithelium is stratified ciliated columnar. 
The submucosa is replete with a venous network, giving it, par- 
ticularly over the inferior turbinated bone, the appearance of 
erectile tissue. In the olfactory regions non-ciliated columnar 
cells, which become attenuated at the inner end, line the surface. 
Between the filiform prolongations within lie round and tapering 
olfactory cells. Small tubular and racemose serous and mucous 
glands are freely distributed in the mucosa. 

CONGENITAL ABNORMALITIES. 

Deviations of the septum and other slight anomalies are com- 
mon. Atresia, absence of the septum or other parts, or complete 
absence of the nose, are rare defects. Harelip and cleft palate 
frequently involve the nasal cavities. 

CIRCULATORY DISTURBANCES. 

Active congestion occurs in consequence of exposure to 
great heat or cold, or of ascending elevations ; and when the heart 
is overstimulated. 

Passive congestion may be due to cardiac weakness, obstruc- 
tive diseases of the lungs, and local pressure on veins. 

Hemorrhage. — In either passive or active congestion hemor- 
rhage (epistaxis) may occur. Bleeding may, however, result from 
blood-diseases (hemophilia, pernicious anemia, leukemia), from 
disease of the blood-vessels (arteriosclerosis), or in a paroxysmal 
form from obscure causes. Epistaxis is a frequent prodromal 
symptom of typhoid fever ; less frequently it occurs in influenza 
and other infections. 

Kdema of the mucous membrane may be associated with in- 
flammation. 

INFLAMMATIONS. 

Acute nasal catarrh (acute rhinitis ; coryza) commonly 
results from exposure to cold. Irritant fumes may cause it ; often 
it seems infectious and contagious. It may occur as an associated 



DISEASES OF THE RESPIRATORY SYSTEM. 



419 



condition in various infections, as grip, typhoid fever, measles, etc. 
The mucosa is at first intensely red and dry ; then an irritating 
serous, followed by mucous and finally mucopurulent, exudation 
is discharged. Herpes or eczematous eruptions of the lip are 
common. Considerable inflammatory edema of the mucous mem- 
brane of the nose and accessory cavities may occur. 

Chronic rhinitis follows repeated acute attacks, especially 
in scrofulous, tuberculous, or syphilitic persons. The mucosa, 
especially over the inferior turbinated bone, becomes thickened 
(hypertrophic rhinitis) and may remain so, or undergo atrophy 
(rhinitis atrophica). In the latter the exudate is scanty and ap- 
pears as dry, greenish crusts, which sometimes occasion extensive 
ulcerations and become horribly offensive. To such cases the term 
ozena is applied. Various forms of bacilli and micrococci have 
been discovered, the most frequent being an organism resembling 
the bacillus of Friedlander. Fetid discharges may also occur in 
syphilitic or tuberculous diseases of the nose (ozoena syphilitica s. 
tuberculosa). 

INFECTIOUS DISEASES. 

Diphtheritic rhinitis is usually secondary to pharyngeal 
diphtheria. Primary diphtheritic rhinitis of rather benign char- 
acter is occasionally observed. Non-specific diphtheritic rhinitis 
is a very rare condition. 

Syphilis in the secondary stage and in congenital cases some- 
times occasions simple catarrhal rhinitis. Mucous patches may 
occur, or gummata springing from the mucous membrane or from 
the periosteum or perichondrium. The latter tend to ulcerate and 
cause destruction. The purulent discharge may be fetid. 

Tuberculosis may occur as disseminated or aggregated 
tubercles of the mucous membrane, or as ulcers and carious pro- 
cesses. These are all rare, but " scrofulous catarrhs " of children, 
probably often tuberculous, are common. Lupus of the face may 
extend to the nose. 

Glanders occasions intense purulent and hemorrhagic rhinitis, or nodu- 
lar growths with ulceration. Nodules and ulcers in lepra, and irregular 
swelling and induration of the mucous membrane of the nose and the 
adjoining skin in rhinoscleroma are rare conditions. 

TUMORS. 

The commonest form of tumors is the 'polyp, which is some- 
times distinctly the result of hypertrophic rhinitis, at other times 
obscure in origin. Polyps present the ordinary structure of the 
nasal mucosa, with a tendency to cystic change from occlusion of 
the glands, or to adenomatous appearances from proliferation of 
the glandular elements. Fibroid, myxomatous, and sarcomatous 
polyps also occur. In all cases there is a tendency to recurrence 



420 



TEXT-BOOK OF PATHOLOGY. 



after removal. A rare form of hairy polyp has been recently 
described. Chondromata, osteomata, sarcomata, and epithelial or 
glandular cancers may be found. 

PARASITES AND FOREIGN BODIES. 

Larvae of various flies may occur in the nasal chambers and set 
up serious inflammatory lesions. Foreign bodies may become 
incrusted with lime-salts and lead to the formation of rhinoliths. 

THE LARYNX. 

Anatomic Considerations.— The lining epithelium of the 
larynx is stratified squamous as far as the false vocal cords. 
Below these and throughout the ventricles it is stratified ciliated 
columnar, and thus continues into the trachea and bronchi, ex- 
cepting over the true vocal cords, which are covered with strati- 
fied squamous epithelium. The tunica propria contains much 
yellow elastic fiber, and the submucosa is quite loose, especially 
over the base of the epiglottis and the aryepiglottic folds. 

CONGENITAL ABNORMALITIES. 

Minor defects in shape of the constituent parts of the larynx 
are not rare. Congenital fistula? communicating with the exterior, 
and dilatation of the ventricles similar to the normal pouching 
found in certain monkeys, are occasionally met with. Abnormal 
largeness and smallness, the latter especially in persons having 
poorly developed sexual organs and those castrated early in life, 
are more frequent conditions. 

CIRCULATORY DISTURBANCES. 

Anemia may occur in general anemia, and is sometimes found 
in tuberculous and chlorotic subjects in pronounced degrees. 

Active hyperemia follows exposure, overuse of the voice, 
and irritation by gases, dust, and the like. 

Passive hyperemia occurs in heart-diseases, intrathoracic 
tumor, and other conditions obstructing the venous circulation. 
In active congestion the larynx is bright red ; in passive con- 
gestion it is dark red in color, and distended veins may be 
prominent. 

Hemorrhages are seen in the mucosa after death from 
asphyxia, in cases of purpura or other hemorrhagic conditions, as 
well as in intense inflammation of the larynx. Large hemor- 
rhages may occur in cases of cancer. 

I$dema of the epiglottis, the aryepiglottic folds, and other 
parts of the larynx may be part of a general anasarca in Bright's 



DISEASES OF THE RESPIRATORY SYSTEM, 421 



disease or heart-disease, or may result from local pressure upon 
the veins. The parts become greatly swollen, and of an anemic, 
translucent appearance. Great stenosis of the laryilx commonly 
results. Generally " edema of the larynx " is inflammatory in 
nature (see below). 

INFLAMMATIONS. 

Acute catarrhal laryngitis results from chemical or 
mechanical irritation ; it accompanies whooping-cough, measles, 
small-pox, typhoid fever, and other infections. The mucous 
membrane is bright red and swollen. A scanty mucous or muco- 
purulent exudate is usually noted. Intense laryngitis is attended 
with small hemorrhagic ecchymoses or erosions ; true ulcers are 
rare. Follicular ulcers are sometimes seen, and rarely small 
vesicles arise upon the surface (herpetic laryngitis). 

Pathologic Physiology. — Acute laryngitis may cause consider- 
able disturbance of breathing by the swelling of the mucous mem- 
brane, and in children often leads to spasmodic contraction of the 
laryngeal muscles, with paroxysmal dyspnea (false croup). 

Chronic catarrhal laryngitis may follow the acute form, or 
begin gradually. Overuse of the voice and exposure to cold or 
irritating gases or dust are the common causes. The mucous 
membrane is usually thickened and somewhat granular, or even 
papillomatous. There is a tendency for the epithelium to assume 
a squamous or epidermoid character, especially on the vocal cords 
(pachydermia laryngis). In the later stages atrophic changes 
may ensue. 

Edematous laryngitis is generally known as edema of the 
larynx. Nearly always it is a true inflammatory edema, due to 
violent irritation, general or local infection, or severe local lesions 
of a chronic nature, such as tuberculous or syphilitic ulceration 
and perichondritis. The looser submucous tissues at the base of 
the epiglottis and over the aryepiglottic folds become greatly 
swollen, and the surface is more or less translucent. Sometimes 
the edematous infiltration is yellowish, or even quite purulent, 
especially in cases in which phlegmonous suppurations have ex- 
tended from neighboring parts (retropharyngeal abscess ; erysipe- 
las). When circumscribed areas are affected abscess results. 

Perichondritis, inflammation of the perichondrium of the 
cartilages of the larynx, is usually secondary to serious laryngeal 
diseases, as syphilitic or tuberculous ulcers, carcinoma, etc. It 
may be primary in typhoid fever or other infections. Frequently 
suppuration and necrosis of the cartilage result ; but merely local- 
ized induration and swelling may occur. 



422 



TEXT-BOOK OF PATHOLOGY. 



INFECTIOUS DISEASES. 



Diphtheritic and croupous inflammations may be part 

of the anatomical changes in diphtheria, but may also occur in 

typhoid fever, scarlet fever, 
small-pox, or other infectious 
diseases, or from violent irri- 
tation by steam or the like. 
The surface of the larynx is 
covered with a more or less 
adherent, grayish or yellowish 
pseudomembrane, which con- 
sists of a network or masses 
of fibrin entangling degener- 
ated round cells and epithe- 
lium. The membrane is most 
adherent where the epithelium 
is squamous. Diphtheritic 
laryngitis usually follows a 
similar process in the pharynx 
(see Diphtheria, Part I.). 

Tuberculosis is nearly 
always secondary to pulmo- 
nary tuberculosis. Small lo- 
calized tuberculous masses, or 
more diffuse tuberculous infil- 
tration, are found in the mu- 
cosa and submucosa, especially 
on the posterior wall of the 
larynx. Early caseation and 
ulceration are further charac- 
teristics (Fig. 192). Simple 
catarrhal inflammation, or hy- 
pertrophic conditions of the mucous membrane between the 
tuberculous masses, or edematous laryngitis and perichondritis, 
may complicate the tuberculous lesions. Lupus of the nose and 
pharynx may extend to the larynx, where it occasions nodular thick- 
enings and ulceration. Primary laryngeal lupus has been observed. 

Syphilis may occasion simple catarrh of the larynx, or infil- 
tration and erosion of the mucous membrane secondary to pharyn- 
geal involvement. The latter conditions are most frequent in 
the epiglottis, the posterior wall of the larynx, and the vocal 
cords. Gummata may occur in the same situations independent 
of pharyngeal syphilis, and lead to deeper ulcers. In the 
healing of syphilitic ulcers irregular papillomatous elevations 
of the healthy mucosa, or extreme contractions and deformities 
of the larynx, may occur. 




Fig. 192.— Tuberculous erosion and ulcer- 
ation of the larynx, causing extensive de- 
struction of the vocal cords (from a specimen 
in the Museum of the Philadelphia Hospital). 



DISEASES OF THE RESPIRATORY SYSTEM. 423 



I^epra and glanders sometimes occur in the form of nodular 
swellings and ulcers. 

Swelling and ulceration of the lymphatic follicles analogous to 
the lesions in the intestines may occur in typhoid fever ; and in 
small-pox there may be small areas of infiltration and epithelial 
degeneration, or even pseudomembranes. 



TUMORS. 

Papilloma. — Over half of all tumors of the larynx belong to 
the group of papillomata or papillomatous fibromata. These are 
simply hypertrophied papillae covered Avith a thick mantle of 
squamous epithelium (Fig. 193). The 
stroma may be insignificant and the 
epithelium considerable (hard papilloma), 
or the stroma may be excessive, highly 
vascular, and infiltrated with round cells, 
while the epithelial covering is thin (soft 
papilloma). Papillomata are most frequent 
on the false vocal cords or on the other 
parts of the larynx lined with squamous 
epithelium. They usually occur in num- 
bers, but may be solitary. Chronic in- 
flammation often determines their occur- 
rence ; and they are not infrequent around 
chronic ulcers or carcinoma of the larynx. 
Simple hyperplasia of mucous membrane, 
of normal structure, occurs in various 
chronic inflammatory conditions of the 
larynx. 

Fibroma. — Nodular, sessile, or poly- 
poid fibromata constitute one-third of all 
tumors. They are most frequent on the 
upper part of the larynx. 

Cystic dilatation of the glands may occasion mucous polyps. 
Adenoma, lipoma, myxoma, sarcoma, and chondroma are rare 
tumors. Tumor-like masses of heterotopic thyroid-gland tissue 
lave been found in the larynx. 

Carcinoma may be primary, or less frequently secondary. 
Primary carcinoma is usually of the squamous variety and occurs 
about the vocal cords. Nodular thickening with ulceration results. 
Papillomatous thickening of the mucous membrane frequently sur- 
rounds the growth. Secondary involvement of the cervical glands 
and esophagus may occur. 

Of 1100 tumors of the larynx, collected by Brims, 602 were papillo- 
mata, 346 fibromata, 73 mucous polyps, and 27 cysts. Seventy-six per cent, 
occupied the true cords, or the anterior commissure of the cords. Mackenzie 
found 67 per cent, papillomata and 16 per cent, fibromata. 




Fig. 193— Papillomata of 
the vocal cords (from a speci- 
men in the Museum of the 
Philadelphia Hospital). 

r ocal cords and in the 



424 



TEXT-BOOK OF PATHOLOGY. 



PARASITES AND FOREIGN BODIES. 

The larval Trichina spiralis may infest the laryngeal muscles 
and lumbricoids occasionally enter from the pharynx. jEchino- 
coccus cysts are very rare. 

Large foreign bodies may cause death by suffocation. Smaller 
bodies may rest in the larynx, especially the ventricles, for years, 
becoming surrounded by hyperplastic mucous membrane or a cap- 
sule of fibrous tissue. Calcareous concretions may form around 
small foreign bodies, or spontaneously in the ventricles. 

THE TRACHEA. 
MALFORMATIONS. 

Congenital Malformations. — Complete absence of the 
trachea occurs in acephalic monsters. Congenital decrease in 
length or diameter, in the number or completeness of the carti- 
lages, and like minor deformities, are more common. An adven- 
titious bronchus is occasionally seen, especially on the right side, 
and fistulous communications with the exterior or with the esopha- 
gus are rare congenital defects. Diverticula may be due to a 
rudimentary condition of a supernumerary bronchus. Congenital 
cysts may occur between the trachea and esophagus when fistulous 
communications between them become closed at either end. 

Acquired Malformations.— Dilatations of the trachea may 
be diffuse or localized. They depend for their occurrence upon 
weakness of the walls and some impediment to expiration. Sac- 
cular dilatations are usually on the posterior wall. Narrowing of 
the lumen may be due to pressure of tumors or aneurysms ; to 
new growths or cicatricial contractions (especially syphilitic) or 
to foreign bodies within. 

CIRCULATORY DISTURBANCES. 

Anemia and active and passive congestion result from the same 
causes as in the larynx ; and the pathologic anatomy is the same. 

INFLAMMATIONS. 

Inflammations are usually associated with laryngitis or bron- 
chitis, and are due to the same causes. Simple catarrhal and pseudo- 
membranous inflammations are met with. Foreign bodies may 
cause extensive and deep inflammation, leading to ulceration and 
sometimes perforation. Chronic inflammation assumes a prolifera- 
tive, and later an atrophic, character. Proliferative (polypoid) 
inflammation is not infrequent after tracheotomy, and may occa- 
sion serious obstruction. Ozena of the trachea may be associated 
with nasal ozena. 



DISEASES OF THE RESPIRATORY SYSTEM. 425 



INFECTIOUS DISEASES. 

Tuberculosis and syphilis occur under the same circum- 
stances as in the larynx. Syphilis may, however, affect the 
trachea and bronchi independent of disease of the pharynx or 
larynx. 

TUMORS. 

Primary tumors are rare. Secondary involvement by cancer, 
extending from the esophagus or thyroid gland, or by sarcoma, 
from the surrounding lymphatic structures or thymus gland, is 
more frequent. Ecchond roses and osteomata may spring from the 
cartilages, and multiple chondromata have been found in the mu- 
cous membrane. Retention-cysts of the mucous glands are occa- 
sionally seen on the posterior wall, protruding outside the trachea. 

THE BRONCHI. 

Anatomic Considerations. — The larger bronchi corre- 
spond very closely to the trachea in structure. The smaller 
divisions have thinner walls, being less provided with cartilagi- 
nous rings, but having instead small cartilage-plates and greater 
abundance of muscle-fibers. The tubes having a diameter less than 
1 mm. are called the terminal bronchioles, and lead into yet smaller 
tubes, the alveolar passages, which open into dilated infundibula, 
and the last named are finally surrounded by air-sacs. The lining 
epithelium is stratified columnar ciliated down to the terminal 
bronchioles, where it becomes simple columnar. In the alveolar 
passages there is first polygonal, then flat, epithelium ; while in the 
infundibula and air-sacs there are practically only flat epithelial 
cells. 

CONGENITAL MALFORMATIONS. 

These are rare and unimportant. Dilatations or narrowing and 
anomalous division of the tubes have been noted (see Trachea). 

CIRCULATORY DISTURBANCES. 

Anemia and hyperemia occur under the same circumstances 
as in the trachea and larynx. 

Hemorrhage. — Intense congestion may occasion hemorrhages 
into the mucous membrane or into the bronchi themselves. More 
frequently hemorrhage is due to catarrhal inflammation, tuberculous 
ulceration, or a general hemorrhagic tendency. Aneurysms of the 
aorta (see Fig. 188) and the small aneurysms of the pulmonary 
arterioles in tuberculosis of the lungs not infrequently rupture 
through the bronchi. 

INFLAMMATIONS. 

Both acute and chronic bronchitis are common conditions, and 
there are a variety of forms. 



426 



TEXT-BOOK OF PATHOLOGY. 



Acute catarrhal bronchitis results from exposure, from 
inhalation of irritating gases, and from downward extension of 
tracheal catarrhs. The terminal bronchioles are frequently affected 
secondarily in pulmonary diseases. Bronchitis is constantly asso- 
ciated with some of the infectious fevers — typhoid fever, measles, 
whooping-cough, etc. Various micro-organisms have been found 
in bronchitis. Among these are the pyogenic micrococci, the 
diplococcus of Frankel, the bacillus of Friedlander, and latterly 
the Bacillus influenzae, the Bacilli coli, with many others. The 
mucous membrane presents an intensely red color; at first it 
is dry, but later a mucous or mucopurulent exudate is formed 




Fig. 194.— Acute bronchial catarrh (Thoma). 



(Fig. 194). The exudation may be excessive in quantity, in which 
case the condition is called bronchorrhea. This may be serous or 
purulent, and is sometimes very offensive in odor {fetid bronchitis). 
Microscopically the bronchial mucous membrane is infiltrated with 
round cells, especially in the purulent cases ; the epithelial cells are 
degenerated, many being converted into goblet-cells ; and the 
mucous glands are distended with mucus. The inflammatory 
conditions may extend outward as far as the peribronchial tissue, 
and occasionally there is some perichondritis. 

Pathologic Physiology. — Bronchitis may occasion no other 
disturbance than cough. In many cases, however, the infection 
may cause fever and general depression. Substernal soreness or 
pain is not infrequent, while generalized thoracic pain may result 
from the violent coughing. Dyspnea is rare excepting in chil- 
dren and old persons, in whom cardiac weakness and spasmodic 
contractions of the bronchi seem to be operative. 

Chronic catarrhal bronchitis occurs after repeated attacks 



DISEASES OF THE RESPIRATORY SYSTEM. 427 



of the acute form, and especially in old persons or in those who 
have some cardiac weakness which tends to cause congestion of 
the bronchi. Chronic bronchitis is frequently associated with 
chronic diseases of the lungs. 
In chronic cases the mucous 
membrane may undergo con- 
siderable alteration. Fre- 
quently the ciliated cells dis- 
appear entirely and are re- 
placed by columnar or polyg- 
onal epithelium ; and hyper- 
trophic conditions of the 
mucous membrane are some- 
times present. More fre- 
quently the bronchus is uni- 
formly thickened by cellular 
infiltration and overgrowth 
of fibrous tissue. 

Fibrinous bronchitis 
occurs under a variety of 
conditions. It is most fre- 
quent in association with fig. 
laryngeal and tracheal diph- 
theria, but may also be due 
to inhalation of powerful irritants. 




195— Large bronchial coagulum; chronic 
fibrinous bronchitis (Vierordt). 



Croupous inflammation of the 




Fig. 196.— Sputum from a case of Fig. 197.— Sputum from a case ot 

asthma, showing Curschmann spirals, asthma, showing leukocytes, some con- 

Charcot-Leyden crystals, leukocytes, and taining eosinophile granules ; freeeosino- 

numerous free eosinophile granules; un- phile granules ; and micrococci; stained 

stained specimen (Jakob). with eosin and methylene-blue (Jakob). 



finer bronchi occurs in both croupous and catarrhal pneumonia. 
Finally, there is a form of chronic or essential fibrinous bronchitis, 



428 



TEXT-BOOK OF PATHOLOGY. 



characterized by periodical attacks, in which fibrinous casts of the 
bronchi are formed and discharged (Fig. 195). In all forms of 
fibrinous bronchitis there are often found in the . sputa, on micro- 
scopic examination, fine spirals wound about a central tiber 
( Curschmann's spi?*als) ; and within these or associated with them 
the small octahedral crystals described by Charcot and Leyden. 

Bronchiolitis Exudativa. — This term was given by Curschmann to the 
condition of the terminal bronchioles he assumed to be present in cases of 
asthma. The sputa contain the spirals that bear his name, and Charcot- 
Leyden crystals. The sputa in these cases are further characterized by the 
abundance of eosinophile cells (Figs. 196 and 197). 

Ulcers of the bronchi are met with in severe catarrhal inflammations, 
but more frequently are tuberculous, syphilitic, or due to extension of ul- 
cerative processes from neighboring parts. It is not unusual to find ulcera- 
tion in the main bronchus opposite the point of pressure of an aneurysm. 

Peribronchitis may occur from direct extension of inflammation from 
within, or it may be due to extension along the lymphatic channels from 
the pleura or interlobular septa of the lung. It is found most frequently 
as a part of pulmonary tuberculosis, and may be fibrous, caseous, or purulent. 

STENOSIS AND OBSTRUCTION OF THE BRONCHI. 

The smaller bronchial tubes may be considerably occluded by 
catarrhal swelling of the mucosa and accumulation of exudate 
within. Clinically this is often so marked in bronchitis affecting 
the terminal bronchioles as to have suggested the name suffocative 
catarrh. (This capillary bronchitis is always merely a part of 
bronchopneumonia, and will be considered under that head.) 
More serious obstructions of the bronchi occur when old ulcers 
have healed, leaving cicatrices ; or in cases of tumors of the bronchi 
or pressure upon the outside. Foreign bodies are usually coughed 
up, but may remain for long periods and occasion obstruction. 

BRONCHIECTASIS, OR DILATATION OF THE BRONCHI. 

This is due to increased pressure within the bronchi or to some 
weakness of the walls, or to both. The weakening of the walls 
is most frequently due to chronic bronchitis. If it is extreme, 
simply the force of the inspired air may suffice to cause dilatation, 
but the increased expiratory efforts of coughing may aid materially. 
When a part of the lung is collapsed (atelectasis) the impediment 
to the entrance of air leads to dilatations of the bronchi above the 
collapsed area. This is especially noted in children. The weight 
of accumulating secretions in the tubes is rarely the cause of 
bronchiectasis. Finally, in fibrous pneumonia the traction of the 
connective tissue, attaching itself, on the one hand, to the outer 
wall of the bronchus, and, on the other hand, to the pleura, may 
bring about considerable dilatations. 

The enlargement of the bronchus may be localized, when it 



DISEASES OF THE RESPIRATORY SYSTEM. 429 



is termed saccular bronchiectasis; or more uniform, when the 
names cylindrical and fusiform are applied, according to the shape 
of the bronchus (Fig. 198). The mucous membrane may be 
almost normal in appearance in small dilatations, but more com- 
monly is thickened and irregular on the surface. There may even 



b 




Fig. 198.— Bronchiectasis : a, saccular; b, cylindrical ; one-half natural size (Orth). 

be actual polypoid outgrowths, and ulcerations may occur when 
the secretions are specially abundant and irritating. Microscopi- 
cally the epithelium is found to approach the squamous type ; while 
the wall of the bronchus is generally infiltrated and cirrhotic. 
The exudation is generally purulent and copious, and may be 
very fetid. Occasionally it is thick and cheesy. 

INFECTIOUS DISEASES. 

Tuberculosis of the bronchi is usually associated with pul- 
monary tuberculosis, and appears in the form of miliary or larger 
nodules in the mucosa or submucosa, which tend to break down to 
form ulcers. 

Syphilis sometimes occurs in the form of eruptions and ulcers. 
There may be dense scar-formation and deformity in consequence 
of the healing of such ulcers. 

TUMORS. 

Polypoid conditions of the mucosa occur in cases of chronic 
bronchitis. Fibroma, chondroma, and lipoma are rare forms of 
tumors. Primary cancers may spring from the mucous glands, 
or from the surface-epithelium, but are very rare. Leukemic 
nodules are seen in the bronchi at times, and lymphosarcomata are 
not rarely found to spring from the peribronchial lymphatic tissues. 

PARASITES AND FOREIGN BODIES. 

Bronchiectatic cavities may contain a growth of aspergillus — 
Mycosis aspergilhna. Round worms may enter by migration, and 
hydatid cysts are met with. 



430 



TEXT-BOOK OF PATHOLOGY. 



Foreign bodies from the exterior usually enter the right bron- 
chus. They often lead to serious inflammation and suppuration, 
unless they are coughed up. Bronchial concretions sometimes 
form by inspissation of the secretions, especially in bronchiectatic 
cavities. Very rarely cartilaginous or bony masses, derived by 
outgrowth and later separation from the bronchial cartilages, are 
observed. 

THE LUNGS. 

Anatomic Considerations.— The structure of the lungs in 
their unexpanded condition is very similar to that of an epithe- 
lial gland, consisting of ducts, the bronchi ; and glandular tissue, 
the pulmonary parenchyma. The terminal bronchioles divide 
into several alveolar passages, which open into infundibula, and 
these in turn are surrounded by air-sacs. The groups of infun- 
dibula connected with a terminal bronchiole constitute an acinus. 
Neighboring acini unite to form lobules, and the lobules unite to 
form lobes. The epithelial lining-cells of the air-sacs are large, 
flat plates, which resemble endothelial cells very closely. Beneath 
these cells is a layer of elastic tissue, which gives the lungs their 
characteristic elasticity, and in Avhich is embedded a rich network 
of capillaries, that carry on the proper respiratory function of 
the lungs. These capillaries are the terminal ends of the pulmo- 
nary artery. Another set of blood-vessels, the bronchial arteries, 
serve only to nourish the walls of the bronchi and the structure 
of the lungs themselves. The return circulation is mainly carried 
on by the pulmonary veins, which receive the blood of the 
pulmonary arteries and much of that of the bronchial arteries. 
The distribution of the lymphatic vessels in the lungs is of the 
greatest significance in pathologic anatomy, especially with regard 
to the dissemination of infectious diseases in the lung itself. One 
system of lymphatics begins in the lymph-spaces between the cells 
of the intervesicular septa. These lymph-spaces deliver their 
contents to lymphatic capillaries in the same region, and these in 
turn follow the alveolar passages, surrounding the latter on all 
sides. Where the several alveolar passages unite to form a ter- 
minal bronchiole the smaller lymphatic capillaries also unite to 
form larger branches, which follow the bronchioles. Other lym- 
phatic vessels surround the pulmonary veins, constituting a peri- 
vascular system. Still another system begins in small subpleural 
capillaries, which unite and enlarge and penetrate the lung along 
the interlobular septa. A portion of them also pass at once to the 
peribronchial and perivesicular tissues. All of the lymphatic 
trunks leave the lung at the root and eventually discharge into 
the thoracic duct. 

Collections of lymphoid cells are found in various places along 



DISEASES OF THE RESPIRATORY SYSTEM. 431 



the lymphatics in the tissue of the lung. Near the root these are 
of considerable size, and merit the name of lymphatic nodes or 
glands. Still larger and more important ones are found surround- 
ing the bronchi just outside the lungs, and around the end of the 
trachea. 

CONGENITAL DEFECTS. 

Complete absence of the lungs has been noted in certain mon- 
sters. One lung may be absent, or its parenchyma may be unde- 
veloped, while the bronchi are dilated even to a cystic condition. 
The opposite lung is compensatorily enlarged. Minor abnormali- 
ties in the division of the lobes and the like are not rare ; and in 
a few instances accessory lobes, wholly disconnected from the rest 
of the lung, have been observed. 

CIRCULATORY DISTURBANCES. 

Anemia of the lung occurs as a part of general anemia, from 
pressure upon the lung, or from obstruction or obliteration of the 
blood-vessels. The last is the cause of the great pulmonary 
anemia in emphysema of the lungs. The lungs are pale in color 
or of a mottled appearance in elderly persons, in whose organs 
considerable pigment is usually present. 




Fig. 199— Acute congestion of the lung (Karg and Schmorl). 



Active Hyperemia or Congestion. — Exercise constantly 
leads to increased flow of blood to the lungs, and this may be ex- 
treme, causing rapid death (apoplexia pulmonum vascularis). In 
cases of irritation of the lungs by the inhalation of heated or cold 
air, or of irritating gases, and in certain lesions of the base of the 
brain, there may be more or less active congestion of the lungs 
(Fig. 199). Collateral hyperemia occurs when the opposite lung 



432 



TEXT-BOOK OF PATHOLOGY. 



or some other part of the body becomes anemic. The lung in 
active hyperemia has a dark-red color, and on section blood flows 
from the surface of section. The alveoli may contain free blood, 
and in marked cases there is blood in the sputa during life. 

Passive hyperemia is for the most part a chronic condition, 
due to causes which prevent the outflow of blood from the lungs. 
The most frequent cause is valvular disease, particularly mitral 
stenosis and regurgitation ; but weakness of the left ventricle 
from fatty disease or fibroid degeneration acts in a similar manner. 
Any local cause of hindrance to the outflow of the blood in the 
veins leads to similar passive congestion. It is often found in 
the dependent parts of the lungs in cases of great asthenia, as in 
typhoid fever. This is called hypostatic congestion; not infre- 
quently it leads to hypostatic pneumonia when irritants are inspired 
or descend through the bronchi to the parts of the lung affected. 
Post-mortem there is often a similar hypostatic congestion, but 
without any evidences of catarrhal inflammation of the bronchi, 
such as always occurs in the cases developed during life. 




Fig. 200.— Phagocytic cells of the sputum, containing blood pigment, from a case of 
cardiac congestion of the lungs (Jakob). 

The lung in passive hyperemia is dark-red in color and heavy. 
In the more acute cases it is moist on section, being infiltrated with 
serous exudate and blood ; in chronic cases, as in slow heart-failure, 
the tissue is dry and indurated. Microscopically the blood-vessels 
in the alveolar walls are seen to be greatly distended, and project 
into the alveoli. Red and white blood-corpuscles are seen within 
the alveoli and in the interstitial tissues. In the later stages the red 
corpuscles either re-enter the circulation or break down to form 
dark pigment-granules within the alveolar epithelial cells, the leu- 
kocytes, or lying free in the tissues of the alveolar walls. In such 
cases there are at the same time considerable hyperplasia and indu- 



DISEASES OF THE RESPIRATORY SYSTEM 433 



ration of the connective tissue of the lung ; and the whole process 
is called cyanotic induration. In cases of heart-disease with con- 
gestion of the lungs there are very commonly found in the sputa 
pigmented epithelial cells and leukocytes, such as those described 
above (Fig. 200l They are of somewhat diagnostic importance. 

Edema occurs most frequently as a result of passive hyperemia. 
In other cases the edema is the consequence of general septic condi- 
tions which lead to unusual permeability of the blood-vessels. In 
this group of cases belong the instances of " acute idiopathic 
edema " which are apparently independent of cardiac weakness 
and probably dependent on some form of infection. Similar 
edema, not dependent on passive congestion, occurs in the parts 
of the lung surrounding inflammatory areas, and in some cases 
sudden pulmonary edema seems dependent on vasomotor relaxa- 
tion. In cases of stenosis of the larynx, edema of the lung may 
result from the reduced pressure of air in the alveoli and the con- 
sequent suction of blood to the pulmonary circulation. In the 
cases of edema due to passive congestion the lungs are dark-red 
in color, and on section more or less serous fluid, rendered frothy 
by admixture of air, exudes from the cut surface. In the 
other forms of edema the lung may be quite light in color, 
generally grayish, but on section the same frothy serum exudes 
from the surface. 

Hemorrhage. — Small punctate hemorrhages occur in cases 
of severe congestion or inflammation, in the hemorrhagic or in- 
fectious diseases, and in consequence of high blood-pressure, as in 
death from asphyxia or in whooping-cough. "When hemorrhage 
from congestion is combined with serous effusion the lung assumes 
an appearance not unlike that of a hyperemic spleen (splenization). 
A form of apparent hemorrhage is seen in cases in which the blood 
is a -pirated from the bronchi. In such cases, lobular spots of 
hemorrhagic infiltration - are found at the bases. Large hemor- 
rhages into the substance of the lungs may be traumatic, or they 
may be due to rupture of an adjacent aneurysm into the lung. 
Small or large pulmonary hemorrhages are at times due to lesions 
of the nervous system, especially of the base of the brain. 

Hemorrhage from the lungs, discharging externally through the 
bronchial tubes, is most commonly due to tuberculosis, and is 
particularly frequent in the late stages, when cavities have formed. 
The immediate source of the bleeding is generally an eroded ves- 
sel in the wall of the cavity, and a small miliary aneurysm is 
commonly found at the point of erosion. Hemoptysis may be the 
first indication of the existence of pulmonary tuberculosis, but the 
old belief that hemorrhages cause phthisis is ill-founded. A 
hemorrhage or any other lesion of the lungs may, of course, add to 
the liability to infection ; but, as a rule, the cases in question are in- 
stances of hemorrhage occurring before the other evidences of the 
pulmonary disease have become marked. Occasionally hemopty- 
. 28 



434 



TEXT-BOOK OF PATHOLOGY. 



sis is due to congestion of the lungs, to erosion of small blood- 
vessels from gangrene, abscess, or the like, or to vicarious men- 
struation. 

Hemorrhagic infarcts may occur in the lungs, as in other 
places, from obstruction of the arteries by emboli. The latter 
come from the right heart or from the general venous system, and 
lodge in the smaller branches of the pulmonary artery, frequently 
at their points of subdivision. Very often, however, emboli are 
not found, or, if so, are so small as to have been unable to cause 
obstruction without the associated thrombosis, or there may be 
purely thrombotic occlusion. Valvular lesions and muscular 
weakness of the heart aid greatly in the production of infarctions 
by causing a sluggish circulation in the pulmonary vessels, and 
thus encouraging thrombosis. Infarctions are occasionally due to 
thrombosis of the pulmonary veins without obstruction of the 
arteries ; more rarely they are caused by occlusion of one of the 
bronchial tubes. The latter condition leads to collapse (atelectasis) 
of the part of the lung associated with that tube, to consequent con- 
gestion (see Atelectasis), and, sometimes, when the congestion is 
severe, to hemorrhage. In addition, it is to be remembered that 
hemorrhages into the lungs are likely to have the shape and appear- 
ances of ordinary infarcts, because they occupy the area supplied by 
the bronchus into which the blood finds its way. Infarctions are 
most frequently found in the lower lobes and in the right lung; they 




Fig. 201.— Hemorrhagic infarction of the lung (from a photograph by Dr. Wm. M. Gray). 

are usually multiple. They have the characteristic wedge-shape, the 
base of the wedge directed toward the pleural surface. They are 
hard, airless, dark -colored, and project above the other parts on 
section and on the pleural surface. Microscopically there is seen 
a uniform hemorrhagic infiltration of the tissues (Fig. 201), and 
not infrequently hyaline thrombosis of the smaller blood-vessels. 
Toward the apex of the infarct there is more fibrin in the blood- 
vessels, and the main vessel may be found obstructed by an embo- 



DISEASES OF THE RESPIRATORY SYSTEM. 435 



lus or thrombus. Small infarcts may be wholly removed through 
the vascular and lymphatic channels after liquefaction and granu- 
lar degeneration of the blood-clot. More commonly a pigmented 
scar is left. Softening and cyst-formation may occur, or in cases 
in which the original embolus was infected by micro-organisms, or 
in which the infarct becomes infected through the bronchial tubes, 
abscess or gangrene may result. 

Embolism without infarction is not infrequent in the lungs. 
An interesting form is fat-embolism, resulting from fracture of a 
bone with disorganization of the marrow, and less frequently from 
traumatic disturbances of other fat-tissues. When large branches 
of the pulmonary artery are occluded in this way, or when numer- 
ous vessels are obstructed, sudden death may result. In other 
cases there are merely great dyspnea and oppression. Air-embo- 
lism, embolism of hydatid cysts, and embolism of portions of 
tumors are rare. Attention has been called to the embolism of 
placental cells in certain cases of eclampsia. 

HYPERTROPHY AND ATROPHY. 

Hypertrophy. — True hypertrophy, in the sense of increase 
of all the constituents of the lung-tissue, is extremely rare, and 
probably only occurs when areas of the pulmonary tissue have 
been rendered useless early in infancy or in fetal life. Cases have 
been observed, however, in which a single lung occupied the entire 
side of the thorax to which it belonged, and also a part of the 
other side, where complete atrophy of the other lung had existed. 
It may be that limited areas of hypertrophy occur more frequently 
than we at present believe, but evidence is wanting. 

Partial Hypertrophy. — The muscular tissue of the inter vesicular 
septa and of the smaller bronchioles not infrequently undergoes 
proliferation or hyperplasia when there has been obstruction in 
the air-passages, so that greater expiratory force was required. 
Similarly the elastic tissues may become increased ; but these are 
not instances of true hypertrophy. 

Atrophy. — Aside from that which occurs as a part of emphy- 
sema, atrophy does not take place. 

EMPHYSEMA. 

By this term is indicated an increase of the air contained within 
the lungs, either in the normal tubes and alveoli, or in the inter- 
stitial connective tissue. Two varieties of emphysema may be 
distinguished by their essentially different nature. These are the 
interstitial and the vesicular. 

Interstitial emphysema of the lungs is similar to the em- 
physema of the subcutaneous tissues — i. e., the term refers to the 
existence of air within the fibrous tissue of the lung. This occurs 
in the course of affections in which there is some obstruction to the 



436 



TEXT-BOOK OF PATHOLOGY. 



expiration, combined with severe coughing or forcible expiratory 
efforts, leading to rupture of the intervesicular septa and extrava- 
sation of air. Degenerative or inflammatory weakness of any part 
of the pulmonary structure would, of course, act as a primary 
cause. Interstitial emphysema is most commonly observed in 
such diseases as whooping-cough and membranous croup ; it may 
also result simply from straining efforts, as in women during labor, 
or from forcibly blowing wind-instruments, etc. The air from the 
ruptured air-vesicle finds its way into the interalveolar and inter- 
vesicular septa, and, passing along these, eventually reaches the 
interlobular and subpleural connective tissue, where it is seen in 
the form of small blebs, movable from place to place. The pro- 
cess may extend to the roots of the lungs, and even to the mediasti- 
nal tissues or to the subcutaneous tissues of the neck. When an air- 
vesicle near the pleural surface ruptures, pneumothorax may result. 

Vesicular emphysema is the term used to designate over- 
distention of the alveoli and air-sacs of the lung. Two factors 
play a part in the causation of this condition : first, increase of the 
pressure under which the air exists in the lung ; and, secondly, 
degenerative or inflammatory weakness, with loss of elasticity of 
the lung-structure itself. There are several varieties, and the 
causes vary somewhat in each. 

(a) Acute vesicular emphysema results simply from excessive 
air-pressure within the alveoli, and may be more or less wide- 
spread. It occurs in cases in which inflammatory swelling or mu- 
cous secretions within the bronchi obstruct the expiration of air, 
but are not sufficient to impede the more vigorous inspiratory 
force. There results overdistention of the alveoli and air-vesicles. 
Somewhat similar conditions are present when the entrance of air 
into certain parts is impeded by obstruction or disease of the 
bronchi or by consolidations of the pulmonary tissue. Localized 
emphysema of other parts results (Fig. 203) ; the term vicarious 
emphysema is applied to such cases. This is not unusual in the 
lobules of the lung surrounding areas of pneumonic or tuberculous 
consolidation, and may affect an entire lobe or lung when the en- 
trance of air into the other lobes or the other lung is prevented. 

Pathologic Anatomy. — In these cases of acute and vicarious 
emphysema there is simply overdistention of the alveoli, and the 
tissue presents a paler color than normal and a cotton-like sensa- 
tion when grasped in the fingers. Microscopically nothing beyond 
overstretching of the septa and some anemia of the vessels is 
apparent. If the causes continue to operate, changes similar to 
those found in chronic vesicular emphysema ensue. 

(6) Chronic vesicular emphysema is the ordinary form of emphy- 
sema, and is sometimes spoken of as substantial emphysema. 

Etiology. — Chronic vesicular emphysema commonly occurs in 
elderly persons, and is predisposed to by attacks of broncho- 
pneumonia and by the existence of other inflammatory and con- 



DISEASES OF THE RESPIRATORY SYSTEM. 437 



gestive conditions of the lungs. These conditions lead to weak- 
ness and loss of elasticity of the pulmonary tissue. Heredity 
plays a part in the same direction, and it is supposed by some that 
there is an abnormal lack of development of the elastic tissue in 
the lungs of such persons, rendering them more susceptible to this 
disease. The direct exciting cause of emphysema is increase of 
the air-pressure within the alveoli, and much speculation has been 
indulged in to discover whether inspiration or expiration plays the 
more important part in increasing the pressure. It seems likely 
that the expiratory force is the more important one, as in the case 
of constant coughing in chronic bronchitis, the blowing of wind- 
instruments, and the constant straining in certain pelvic disorders, 
all of which may lead to emphysema. 

Pathologic Anatomy. — The lung increases in size, and very 
often remains distended when the thorax is opened post-mortem. 
The edges are rounded ; the organ is light in color, and has a cotton- 




Fig. 202.— Emphysema of the lungs (Karg and Schmorl). 



like feeling when squeezed between the fingers. On section into it 
the alveoli may be seen to be distended, and there may be cavities 
of quite considerable size, often as large as a pea, and sometimes 
even that of a cherry or plum (Fig. 202). Large spaces of this 
kind are not unusual near the pleural surface ; the term bullous em- 
physema has been used in reference to such cases. The pigment- 
matter of the lung is very much lessened, and may be distributed 
in radiating or parallel lines. This lessening of the pigment is 
not alone due to its distribution over a greater space, but there is 
also actual disappearance by removal through the lymphatic chan- 
nels and through expectoration. 

Chronic emphysema may be a general process affecting all 
parts of both lungs, or it may be localized. In the latter case it 
is the apex and anterior edges that are most commonly involved, 



438 



TEXT-BOOK OF PATHOLOGY. 



but spots of emphysema may be seen here and there in other parts 
of the lung, interspersed with normal tissue. The involvement of the 
apex and anterior portions is due to the fact that the expiratory 
force is more apt to distend these portions of the lung than the 
lateral and basal portions, which receive the uniform support of 
the sides of the chest and the diaphragm as they contract against 
the lung. 

Microscopically emphysema is found to consist in enlarge- 
ment of the vesicles and alveoli by distention and by atrophy 
and disappearance of the intervesicular and interalveolar septa. 
Studied from the earliest stage, there will be found, first, over- 
distention of the air-sacs, then a gradual thinning, and finally 
vacuolization of the intervesicular septa at their thinnest parts. 
Coincidentally the small capillaries are compressed, and are finally 
converted into hyaline cords. The anemia consequent upon this 
determines additional atrophy and degeneration of the septa and 
fatty degeneration of the loosened epithelium, so that eventually 
the whole of the septum disappears. Later, adjacent alveoli inter- 
communicate and large spaces are thus formed. 

The obstruction to the pulmonary circulation due to the oblit- 
eration of the capillaries leads to collateral hyperemia of the larger 
branches supplying the bronchi, and thus prolongs the chronic 
bronchitis, which in the first instance may have been the cause of 
the emphysema, Subsequently collateral anastomosis between the 
pulmonary arteries and the bronchial system of blood-vessels is 
established. 

Associated Conditions in Other Organs. — The shape of the 
thorax in emphysema is characteristic. The chest is in a constant 
state of extreme inspiration, the clavicles elevated, the sternum 
protruded, the back arched. It has a shape well likened to that 
of a barrel. The diaphragm is usually depressed, and the liver is 
below its normal position ; the heart is almost or completely cov- 
ered over in front and usually pressed somewhat backward from 
the chest-wall. 

Pathologic Physiology. — The effect of emphysema upon the 
circulation is important. The obstruction of the pulmonary cap- 
illaries leads to increase of pulmonary pressure, and eventually 
hypertrophy of the right heart ; later, dilatation of the right ven- 
tricle ensues, and characteristic cardiac dropsy with general cyano- 
sis may result. 

(c) Senile emphysema is due to erosion of the intervesicular 
septa, the result of the atrophic processes to which old age pre- 
disposes. There is not necessarily any element of increased air- 
pressure in the causation of this form of emphysema, and the 
volume of the lung may not be notably increased, though the 
tissue is lighter and the air-spaces are found to be increased. The 
lung is light in color and often collapses readily. 



DISEASES OF THE RESPIRATORY SYSTEM. 439 



ATELECTASIS. 

The term atelectasis is applied to two distinct conditions, one 
occurring as a congenital affection, in which the lung has never 
been properly expanded by air ; the other occurring in after-life, 
in which the lung is compressed or collapsed, so that the alveoli 
and air-vesicles are rendered airless. 

Congenital atelectasis is found in new-born babes in 
whom the inspiratory power has been so deficient, as the result of 
general weakness or compression of the thorax, or of compression 
of the brain by cerebral hemorrhage, that the lungs, or parts of 
them, have never been expanded. It may also take place in a 
purely mechanical way by obstruction to the air-passages by 
meconium or other foreign matter. 

Pathologic Anatomy. — Congenital atelectasis commonly affects 
the bases and posterior portions of the lung. The area of disease 
is of a dark-reddish color • it is rather tough, and on section pre- 
sents a smooth appearance ; pressure gives no sign of crepitation. 
If a portion be thrown into water, it sinks. Usually a con- 
siderable part of the lung is involved, but sometimes merely 
lobular areas are affected. By inserting a blowpipe into the 
bronchi the lung may be inflated, and resumes its normal ap- 
pearance, provided the condition has not persisted for any length 
of time. If the child does not perish, secondary, changes take 
place. The epithelium of the alveoli degenerates, more or less 
proliferation of the connective tissues of the septa occurs, and the 
pleura over the diseased area is prone to become thickened. The 
atelectatic portion of the lung in such cases remains collapsed ; it is 
smooth on section, free of pigment, and can no longer be inflated. 
Secondary dilatation of the bronchioles and bronchi may ensue. 

It is of interest, in a medicolegal sense, to recognize that atelectasis re- 
sembling the congenital form may be met with in the bodies of infants that 
have lived, breathed, and even cried lustily. The explanation of this is 
that the collapse ensued some time after birth, and that as the lung had 
practically still its fetal characteristics, the resulting atelectasis is the exact 
counterpart of the congenital form. 

Atelectasis in later life occurs under a variety of condi- 
tions. It may simply be the result of compression of the lung by 
pleural effusions, by deformities of the chest, by tumors, aneur- 
ysms, and the like. It may also be met with in cases in which 
the bronchial tubes have become obstructed. The larger bronchi 
may be occluded by the pressure of tumors or aneurysms, or by 
foreign bodies, and the resulting atelectasis is of considerable 
extent; the smaller bronchi and bronchioles are frequently ob- 
structed by intense catarrhal thickening of their mucosa, and in 
consequence lobular areas of atelectasis are developed. The latter 



440 



TEXT-BOOK OF PATHOLOGY. 



is especially frequent as one of the pathologic features of broncho- 
pneumonia (q. v.). 

The explanation of atelectasis as the result of bronchial ob- 
struction has occasioned much discussion, and several theories 
have been proposed. In some cases it is not unlikely that mucous 
secretions within the bronchi may prevent inspiratory entrance of 
air into the lungs without opposing any obstacle to expiration, so 
that collapse is gradually developed. In other cases it is likely 
that both inspiration and expiration are prevented, while the air 
contained within the air-vesicles is gradually absorbed. It is 
claimed that first the oxygen, later the carbonic acid, and finally 

the nitrogen, are absorbed ; the col- 
lapse of the alveoli then becomes 
complete. It is possible, also, that 
atelectasis may be developed as the 
result of the failure of respiratory 
motions on one side, or affecting a 
certain part of the lung. As a re- 
sult of this, the elasticity of the 
pulmonary tissue would gradually 
press the air out of the affected 
area, while new air was not sup- 
plied by inspiration. Such a con- 
dition, however, must be rare. 

Pathologic Anatomy. — The part 
affected by atelectasis is dark in 
color, and is much reduced in size, 
so that when lobular areas are af- 
fected the pleural surface may be 
Fig. 203-Ateiectasis due to bron- considerably depressed (Fig. 203). 

chial obstruction: acute emphysema () n section the Surface is Smooth 
of the unaffected portions of the lung , ,, , , , . 

(Orth). and generally dry, though in some 

instances passive hyperemia, which 
is generally present to some extent, reaches such a grade that 
bloody liquid flows freely from the surface of section. The term 
splenization is properly applied to such cases, whereas the instances 
in which the surface is dry are often spoken of as carnification. 
The lung does not crepitate, and sinks when placed in water. In 
the earlier stages the diseased portion may be inflated through the 
bronchial tubes ; but when the condition has persisted, connective- 
tissue overgrowth springing from the septa causes permanent 
induration and permanent collapse. The lung in such cases is 
hard and of a dark color, due to the deposit of hematogenous pig- 
ment, the result of disintegration of the blood present. The 
bronchi may be compressed, but sometimes atelectatic bronchi- 
ectasis results from the increased pressure of air sustained by the 
bronchi in consequence of the collapsed state of the lung-tissue. 




DISEASES OF THE RESPIRATORY SYSTEM. 441 



INFLAMMATION, OR PNEUMONIA. 

Classification. — Inflammation of the lungs, pneumonia, or 
pneumonitis, may arise in a variety of ways, and present itself in 
a number of widely varying forms, both as to the distribution and 
the nature of the pathologic changes in the pulmonary structure. 
In all cases some irritant is conveyed to the lung either (a) from the 
upper air-passages or external world through the bronchi; (6) 
from some other part of the body through the blood (hematogenic 
pneumonia) ; or (c) from the pleura by direct extension or through 
the lymph-channels (pleurogenic pneumonia). 

Anatomically pneumonia is classified according to the nature 
of the inflammatory products, and there are thus distinguished : 
-fibrinous pneumonia, in which the air-vesicles and terminal bron- 
chioles contain an exudate especially rich in fibrin ; catarrhal, or 
bronchopneumonia, in which the exudate is composed of an albumi- 
nous liquid containing numerous epithelial cells and blood-cor- 
puscles ; purulent pneumonia, in which pus-cells are the note- 
worthy element in the exudate; cheesy pneumonia, in which 
cellular desquamation and cheesy necrosis are prominent ; and 
productive, or fibrous pneumonia, in which there is overgrowth 
of fibrous connective tissue. It is to be remembered, how- 
ever, that mixed cases are of frequent occurrence. Thus in 
many instances localized areas of decided fibrinous pneumonia are 
found in the midst of larger areas of catarrhal pneumonia ; some 
distinctly purulent exudation may be met with in many instances 
of fibrinous or catarrhal pneumonia ; and more or less productive 
inflammation and fibrous overgrowth may be seen in any of the 
other varieties. Typical cases, however, present little mixture of 
the lesions. 

The terms parenchymatous and interstitial pneumonia are 
sometimes employed, but are of doubtful significance. The proper 
parenchyma of the lungs, the alveolar septa, and their contained 
blood-vessels, are never the sole seat of inflammation, and the 
term parenchymatous pneumonia, as usually applied to inflam- 
mations of the lining epithelium of the air-vesicles, is therefore 
misused. It is more proper to call the fibrous variety interstitial 
pneumonia. 

Fibrinous Pneumonia. 

Definition. — Fibrinous, or croupous, or lobar pneumonia is 
an acute infectious form of pneumonia, generally caused by the 
Diplococcus pneumoniae, and usually involving an entire lobe or 
more of one or both lungs. Pathologically it is characterized by 
an exudation within the air-vesicles and terminal bronchioles, 
mainly composed of fibrin ; and clinically the disease is marked 
by a definite and characteristic course. 

Ktiology. — The important factor in the causation of fibrinous 



442 



TEXT-BOOK OF PATHOLOGY. 



pneumonia is the Diplococcus pneumoniae (Frankel-Weichsel- 
baum). This micro-organism is found in the sputa and in the 
lungs of the great majority of cases, and is undoubtedly the cause 
of the pneumonia ; but occasionally other micro-organisms seem 
to occasion typical fibrinous pneumonia. Among these are the 
pneumococcus of Friedlander, streptococci, staphylococci, the 
bacillus of typhoid fever, the bacillus of influenza, and the Bacillus 
coli communis. In some cases in which bacteria other than the 
diplococcus are supposed to be the cause, there is doubtless mixed 
infection ; but it must be accepted at the present time that a num- 
ber of micro-organisms are capable of causing the disease. The 
fibrinous pneumonia which occurs in the course of tuberculosis is 
certainly due to secondary infection, and the same thing frequently 
happens in the course of typhoid fever and influenza, though the 
specific bacilli of these diseases may alone cause pneumonia. 

The micro-organisms usually gain access to the lungs through 
the bronchi. In the case of the Diplococcus pneumoniae the fre- 
quent occurrence of this organism in the mouth and upper respira- 
tory passages furnishes a ready explanation of one source of infec- 
tion. More rarely the bacteria may be directly inspired from 
without, or, exceptionally, they may reach the lungs through the 
circulation. 

There are certain predisposing factors which have long been 
recognized clinically as causes of pneumonia. These probably act 
by rendering the pulmonary tissues less resisting, or by increasing 
the virulence of the diplococci of the mouth. Among these causes 
are exposure to cold, injury of the lungs by traumatism, fatigue, 
and systemic depression. 

(For the description of the Diplococcus, see page 216.) 

Pathologic Anatomy. — The lesions most frequently involve 
the lower lobe of the right lung ; next in order is the lower lobe 
of the left lung ; the apices alone are least frequently involved. 
In all cases there is a tendency to the involvement of a whole 
lobe, and, as a rule, the entire area of disease is affected uniformly 
and simultaneously. There are wide variations, however ; for, on 
the one hand, typical fibrinous pneumonia may occasionally appear 
as a more or less lobular disease (particularly in influenza), and, 
on the other hand, the process may spread from one part of the 
lung to another (pneumonia migrans). In typical cases, not only 
is the process uniformly distributed, but it passes through distinct 
stages : first, of congestion, then of consolidation, and finally of 
resolution. 

Stage of Congestion or Engorgement. — The affected area is dark~ 
red in color ; it is swollen and heavy, and on pressure crepitates 
less than a healthy lung. The pleura over the diseased part is 
dull and lusterless. On section through the lung bloody liquid 
exudes, and when the part is compressed with the fingers this 



DISEASES OF THE RESPIRATORY SYSTEM. 443 



liquid shows few air-bubbles. The condition is simply one of 
intense congestion, with exudation into the alveoli and terminal 
bronchioles of serous liquid and blood-corpuscles (see Fig. 199). 
Microscopically the small blood-vessels of the septa are seen to be 
greatly distended and project inward toward the alveoli. Within 
the latter may be found many red corpuscles, a lesser number of 
leukocytes, and some detached epithelial cells. 

Stage of Consolidation, or Hepatization. — The diseased lung is 




Fig. 204.— Red hepatization of the lung (from a photograph by Dr. Wm. M. Gray). 

now completely solid and liver-like in consistency (hepatization). 
It is swollen, and marked on the surface by indentations of the 




Fig. 205.— Croupous pneumonia ; beginning gray hepatization (Karg and Schmorl). 

ribs. The surface of section is at first red in color (red hepatiza- 
tion, Plate 4), but later becomes white or gray, or in elderly 



444 



TEXT-BOOK OF PATHOLOGY. 



persons (in whom the lungs are usually darkly pigmented from 
inhalation of dust) of a variegated appearance, resembling granite 
(gray hepatization, Plate 5). The cut surface is entirely dry, 
and is finely granular on account of the projection of small 
plugs of fibrin from the alveoli and bronchioles. The pleura 
is generally covered with fibrinous exudation. Microscopically 
the alveoli are found distended with a network or particles of 
fibrin, in which the same cellular constituents as occur in the 
stage of congestion are embedded. The fibrinous network is beau- 

© © 

tifully demonstrated by staining the sections after the method 
of Weigert (Fig. 204). The blood-vessels are less prominent than 




Fig. 206. — Advanced gray hepatization (from a photograph by Dr. Wm. M. Gray). 

in the first stage. As the disease advances to the period of 
gray hepatization the number of leukocytes within the exudate 
increases and the blood-vessels become still less prominent (Figs. 
205 and 206). 

Stage of Resolution. — Gradually softening of the exudate occurs 
and the lung becomes more moist. Puriform liquid may be 
squeezed from the surface of section, or may be seen in the bron- 
chioles and bronchi. Crepitation is re-established. Microscopi- 
cally fatty degeneration of the cells of the exudate is apparent. 
Softening is further contributed to by simple liquefaction. The 
result of these processes is emulsifi cation of the exudate, which is 
finally carried oflP by the lymphatics or expectorated. 

Before the process of resolution is completed the epithelial cells 
of the alveoli and bronchioles proliferate, so as to repair the dis- 
eased portions. At the same time proliferative changes may be 
seen in the tissues of the septa. These conditions exist throughout 
the disease to a slight extent, but become more apparent in the 
stage of resolution. Eventually the lung is restored to its pre- 
vious condition. 

Unusual Characters. — In some cases the pathologic changes 



Plate 4. 




Croupous pneumonia, stage of red hepatization (Bollinger). 



Plate j. 




Croupous pneumonia, stage of gray hepatization (Bollinger). 



DISEASES OF THE RESPIRATORY SYSTEM. 445 



vary somewhat from the typical form described. Not rarely there 
are considerable congestion and even edema of the lung through- 
out the disease ; in drunkards or cachectic individuals the exudate 
is more markedly hemorrhagic than is usually the case ; and some- 
times, particularly in instances accompanied by streptococcosis in- 
fection, the exudate is more cellular than customary. In still 
other cases proliferative changes in the septa are prominent. 

Associated I^esions and Pathologic Physiology. — The 
portions of the lung not involved by the pneumonic process are 
usually somewhat emphysematous and congested ; and edema may 
develop. The latter is, however, not so common as has often been 
assumed. The larger bronchial tubes, as a rule, remain "normal, 
or at most become congested. The finer bronchi are more fre- 
quently hyperemic, and excess of mucus coats the surface. In 
practically every case there is a certain degree of fibrinous pleu- 
risy, either on the external surface of the pleura or between the 
lobes. Extensive pleurisy is rare and serous exudation is un- 
common. The pleurisy is directly attributable to the micro-organ- 
ism which has caused the underlying pneumonia. 

Though fibrinous pneumonia is frequently an entirely local in- 
fection, systemic intoxication is usually present, and general infec- 
tion may further aid to develop widespread pathologic changes. 
Leukocytosis is present in the great majority of cases ; its ab- 
sence is generally significant of unusually intense systemic in- 
toxication. White clots are often detected in fatal cases in the 
chambers of the heart and in the large blood-vessels leaving the 
heart. Cardiac and respiratory embarrassment, often ascribed to 
mechanical causes, such as heart-clot or extensive consolidation, is 
probably in many cases due to the action upon the nervous system 
of the toxins of the disease. Myocardial degenerations aid in pro- 
ducing circulatory weakness. The heart-muscle and the kidneys 
may suffer parenchymatous degeneration, as in other febrile infec- 
tions, and acute exudative inflammation (myocarditis, nephritis) 
may occur in either of these organs. Albuminuria is not infre- 
quent, and albumoses may be found in the urine, especially during 
the stage of resolution. The chlorids of the urine are usually 
diminished. The spleen is enlarged and soft. 

Pericarditis is frequent, and endocarditis, either of the simple 
or of the malignant type, is more common than in any other acute 
infection, excepting rheumatism. Meningitis is occasionally noted. 

Fibrinous or pseudomembranous bronchitis, laryngitis, gastritis, 
colitis, and cystitis are sometimes met with. Inflammations of the 
joints and abscesses in various organs may occur. 

Unusual Terminations. — Secondary infection w T ith pyogenic 
micro-organisms may lead to termination in abscess ; or this result 
may be due to the fact that the pneumonia was primarily caused 
by such micro-organisms. The affected area may suffer gangrene 



446 



TEXT-BOOK OF PATHOLOGY. 



even more commonly than suppuration. Gangrene is especially 
prone to occur when the exudation is distinctly hemorrhagic and 
in cases in which the circulation is specially weak. Finally reso- 
lution may be delayed and productive changes may occur in the 




Fig. 207.— Induration of the lung (carnification) in a case of pneumonia of five weeks' 
duration : a, new connective tissue of the septa ; b, intra-alveolar proliferation of connec- 
tive tissue ; c, desquamated epithelium in the alveoli ; e, new blood-vessels ; /, lining epi- 
thelium of the alveoli (Kaufmann). 

septa and even within the alveoli. There results a solidification 
(carnification) of the lungs, or, as it is termed, fibrous pneumonia 
(Fig. 207). 

Catarrhal Bronchopneumonia. 

Definition. — Catarrhal bronchopneumonia, or lobular pneu- 
monia, is an acute inflammatory affection of the pulmonary tissue, 
occurring in localized areas and consequent upon inflammation of 
the terminal bronchioles. In most, if not all, cases some species 
of bacterium is the immediate cause. Pathologically it is charac- 
terized by inflammation of the terminal bronchioles and by exuda- 
tion into the alveoli of albuminous liquid containing desquamated 
epithelial cells, together with more or less red blood-corpuscles 
and leukocytes ; clinically the disease is marked by an indefinite 
> and irregular course. 

Etiology. — Catarrhal pneumonia may be produced experi- 
mentally in animals by causing them to inhale steam or various 
irritating vapors. Still more characteristic lesions are produced 
when the vapors inhaled hold decomposing organic matter in sus- 
pension. The same result is accomplished by cutting the vagus 
nerves, as a consequence of which the vocal bands and esophagus 
are paralyzed and irritating secretions and particles of food are 
conveyed into the lung by inspiration. In man tumors, en- 
largements of the thyroid gland, or inflammatory exudation, 
may compress the vagi and lead to forms of pneumonia similar 
to the experimental pneumonia of dogs. Somewhat analogously, 



DISEASES OF THE RESPIRATORY SYSTEM. 447 



in the late stages of various diseases particles of food and mucous 
secretions may sink to the dependent parts of the lungs, or may 
be drawn in by the inspiratory air and set up catarrhal pneu- 
monia in the parts already predisposed to inflammation by hy- 
postatic congestion (hypostatic pneumonia). Of the same etio- 
logic sort are the catarrhal pneumonias which occur in diphtheria, 
epithelioma of the larynx, and inflammatory conditions of the 
mouth and pharynx, in which irritating particles are carried to 
the finer bronchi by inspiration (aspiration-pneumonia ; deglu- 
tition-pneumonia). Catarrhal pneumonia of this kind is not in- 
frequent in the new-born as a result of vigorous inspiratory efforts 
made while the head is descending through the vagina. 

Most frequent, however, of all forms of catarrhal broncho- 
pneumonia is that which occurs in the course of measles, whoop- 
ing-cough, influenza, or other infectious fevers attended with 
bronchitis. The manner of involvement of the alveolar structures 
will presently be described ; for the present it may be said that 
the inflammatory process extends from the bronchi by continuity 
and contiguity, or by aspiration of irritating bronchial secretions. 

The immediate cause of catarrhal pneumonia is, in the majority 
of cases, some bacterium. The most frequent is the Diplococcus 
pneumoniae, which occurs in over 50 per cent, of all cases, either 
alone or in combination with the Streptococcus pyogenes, staphy- 
lococci, the pneumococcus of Friedlander, the bacillus of influenza 
or of typhoid fever, or the Bacillus coli communis. Any of the 
other forms named, and especially the pyogenic micrococci, may 
cause catarrhal pneumonia without the diplococcus of Frankel ; 
but in the case of fevers (typhoid fever, influenza) in which the 
specific micro-organisms are found, there is usually mixed infec- 
tion with the Diplococcus pneumoniae. 

Pathologic Anatomy. — The lesions vary somewhat in dif- 
ferent cases, and we may distinguish three important types, the 
simple, or ordinary catarrhal bronchopneumonia, the hypostatic 
form, and aspiration-pneumonia. 

1. Simple Catarrhal Bronchopneumonia. — The lung in such cases 
presents more or less distinct external appearances. On the 
pleural surface may be seen lobular areas of dark- or light-red or 
grayish color, which are somewhat elevated and harder than the 
normal lung. Surrounding these the pulmonary tissue is emphy- 
sematous, while here and there may be seen dark-red or lead-col- 
ered and somewhat depressed areas of pulmonary collapse (atelec- 
tasis). The lung as a whole is crepitant, while the pneumonic and 
atelectatic areas are consolidated and airless, and sink in water. 
On section through the lungs the same general appearances are 
visible, though the consolidated patches are most abundant near 
the surface. Both lungs are, as a rule, involved, and any portion is 
liable to the disease. The smaller and medium-sized bronchi and 



448 



TEXT-BOOK OF PATHOLOGY. 



the bronchioles contain mucopurulent secretion, which may be 
squeezed out; the areas of pneumonic consolidation are smooth 
and moist on the surface of section, or exceptionally somewhat 
granular as a result of admixture of some fibrinous pneumonia. 
Occasionally there may be puriform liquid or small purulent col- 
lections around the bronchiole in the center of the lobule. The 
area of collapse (atelectasis) is dark-red, as a rule, and on pressure 
bloody liquid exudes. 

In the very earliest stages of the disease the lobules of con- 
solidation and collapse may be inflated by inserting a tube into the 
bronchus supplying the part and by blowing gently into it. Later 
this is not possible, as the consolidation increases. At the same 
time it is noted that the consolidated areas become lighter in color, 
until at last they are grayish-yellow ; while the areas of collapse 
become pneumonic and present a similar change of color. 

Microscopically the terminal bronchioles and alveolar passages 
present somewhat swollen walls and contain variable amounts 
of mucous exudate containing desquamated cells. In the areas 




Fig. 208.— Catarrhal pneumonia (Karg and Schmorl). 

of consolidation the alveoli and the air-sacs are filled with liquid 
and variable numbers of epithelial cells, red corpuscles, and leuko- 
cytes (Fig. 208). The liquid is albuminous in nature, as may 
be readily demonstrated by boiling a portion of the tissue. The 
epithelial cells are desquamated from the lining membrane either 
singly or in groups, and there is evidence that active proliferation 
is taking place as well. In most cases the number of red corpus- 
cles and leukocytes is small, but in some instances, particularly in 
cases in which streptococci and staphylococci are operative, the 
exudation may be quite hemorrhagic, or later purulent. The alve- 



DISEASES OF THE RESPIRATORY SYSTEM. 449 



olar septa regularly present considerable round-cell infiltration, 
and the blood-vessels are surrounded by emigrated leukocytes. 
The blood-vessels in the septa are distended and tortuous. 

The atelectatic areas present even greater congestion of the 
blood-vessels, and the alveolar cavities are obliterated by the col- 
lapse of the walls, or contain at most a little hemorrhagic exudate. 
The epithelial cells tend to lose their characteristic shape and 
become cuboidal. 

As resolution advances, the cellular exudate becomes lighter in 
color as a result of fatty degeneration, and eventually it is absorbed 
or expectorated. Coincidently the round-cell infiltration disap- 
pears from the septa, and the pulmonary tissue returns to the 
normal, excepting that the epithelial cells of the alveoli tend to 
remain more or less cuboidal for a time. 

Pathogenesis. — The manner of development of the lesions is 
of considerable interest. In the ordinary catarrhal bronchopneu- 
monia now under discussion there is always a primary bronchitis 
of the terminal bronchioles, a bronchiolitis, or capillary bronchitis, 
as it is termed. This may be spread to the alveolar structure in 
several ways. In most instances, no doubt, the inflammation 
travels downward along the bronchioles to their termination by 
continuity, or outward through their walls to the surrounding 
alveoli by contiguity. In either case there results a patch of 
catarrhal pneumonia surrounding a terminal bronchiole. Less 
commonly the affected lobule first becomes atelectatic and then 
•pneumonic. The atelectasis results from the obstruction of the 
bronchioles by mucus or by their swollen walls, and is due to 
the gradual absorption of the air contained within the alveoli and 
the inability of more to enter (see Atelectasis). Subsequently the 
collapsed area becomes inflamed by the entrance of micro-organisms 
from the bronchioles or by extension of surrounding inflammation. 

Unusual Characters. — Marked variations are seen in the nature 
of the process and in its distribution. In some instances there is 
but little pneumonic consolidation, while the bronchiolitis, or capil- 
lary bronchitis, is a striking feature. In other cases the exudate is 
decidedly hemorrhagic or purulent, and it may in certain areas be 
quite fibrinous. Regarding the distribution, the most striking 
variation is the tendency in some cases to lobar involvement by 
confluence of the lobular areas (pseudolobar form). 

Associated Lesions. — The constant association of bronchitis 
has been sufficiently noted. Pleurisy is less common than in 
fibrinous pneumonia, but the patches near the surface are regularly 
covered with fresh pleural exudation. It has long been recognized 
that purulent pleurisy is more apt to occur after pneumonia in 
children than in adults, and in many of these cases the antecedent 
pneumonia is catarrhal. Widespread toxic and infective lesions 
may occur, as in fibrinous pneumonia. 

29 



450 



TEXT-BOOK OF PATHOLOGY. 



Unusual Terminations. — In cases in which micro-organisms, 
more virulent than usual, cause the pneumonia, suppuration and 
gangrene may result. Fetid and pultaceous foci, or purulent 
collections surrounded by considerable areas of congestion and 
inflammatory edema, result. In other instances the process of 
resolution is slow, and fibroid overgrowth of the septa and pro- 
liferation of connective tissue within the alveoli ensue, with the 
production of more or less extensive sclerotic hardening and con- 
traction of the lung-structure. Within such areas the alveolar 
exudate may lie for a long time as a fatty mass ; but this is very 
unusual ; and true caseation, of which so much was formerly said, 
does not occur. The instances in which this was supposed to 
have occurred were cases of subsequent infection with tubercle- 
bacilli, or cases of tuberculous pneumonia ab initio. 

2. Hypostatic Pneumonia. — The bases and posterior portions of 
the lungs are -commonly involved in these cases. The process 
occurs as a terminal affection in many diseases. It begins as an 
intense hypostatic congestion and hemorrhagic edema of the de- 
pendent parts of the lungs. Subsequently the irritants which 
make their way to the congested area through the bronchi set up 
a form of inflammation of the terminal bronchioles and air-vesicles 
which is largely catarrhal, but more fibrinous than ordinary bron- 
chopneumonia. The inflammatory process is also more diffuse, 
and is at the most insignificant compared with the antecedent and 
associated congestion and edema. 

3. Aspiration-pneumonia. — Of the dust which we constantly in- - 
hale, the greatest part is arrested in the upper air-passages or in 
the larger bronchi, and is expectorated. A part, however, reaches 
the finer bronchi and bronchioles, and sets up a certain amount of 
local irritation and congestion, with desquamation of epithelial 
cells and emigration of leukocytes. Ordinarily these processes are 
exceedingly trivial and can rarely be demonstrated. In persons, 
however, whose occupations (e. g., steel-grinding, coal-mining, 
marble-cutting, etc.) subject them to excessive dust-inhalation the 
pulmonary changes are extensive and severe. This is one form 
of aspiration-bronchopneumonia, but the irritation rarely stops at 
the point of catarrhal inflammation ; on the contrary, the irritant 
particles penetrate the walls of the bronchioles and are distributed 
by the lymphatics, causing fibroid changes of greater or less 
extent. The pneumonia thus produced is therefore more properly 
considered as a form of fibrous pneumonia (q. v.). 

In the course of various affections of the pharynx, larynx, 
trachea, and bronchi, as well as in cases in which through palsy 
of the larynx, or through general depression, particles of food or 
secretions of the mouth enter the air-passages, irritating matters 
may be inspired or "aspirated" into the finer divisions of the 
bronchial system. There results intense local irritation, with 



DISEASES OF THE RESPIRATORY SYSTEM. 



451 



catarrhal inflammation and consolidation. The exudate is largely 
epithelial, but more often serous, hemorrhagic, or purulent than in 
simple catarrhal pneumonia. The condition may be circumscribed 
to small patches, but if large particles are aspirated and the larger 
bronchial tubes are obstructed, widespread consolidation, of the 
character described, results. The inflammatory process in these 
cases of aspiration-pneumonia are habitually intense, and often 
terminate in suppuration or necrosis, with considerable surround- 
ing hyperemia and edema. 

Cheesy or Tuberculous Pneumonia. 

Definition. — Cheesy or tuberculous pneumonia is an acute or 
subacute form of pneumonia caused by the tubercle-bacillus, and 
involving lobular areas or, by confluence of such, an entire lobe or 
lung. Pathologically it is characterized by proliferation and des- 
quamation of epithelial cells, infiltration of the alveolar septa, 
and finally by cheesy necrosis of the area of disease. Clinically 
the disease presents itself as a more or less acute pneumonic 
tuberculosis. Caseous pneumonia is frequently associated with 
miliary or peribronchial tubercles, affecting the alveoli adjacent 
to the tubercles. 

Etiology. — Cheesy pneumonia as an independent condition is 
more common in children than in adults. The immediate cause is 
the tubercle-bacillus. Infection occurs by rupture of a tubercu- 
lous gland or cavity into one of the bronchi and dissemination 
of the infective material throughout the lung. Likewise, bacilli 
may be inhaled from outside, or from tuberculous foci in the bronchi, 
larynx, or nose. In cases of disseminated tuberculosis of the lungs 
areas of caseous pneumonia are habitually encountered in the pul- 
monary structure between the tubercles. Finally, infection may 
take place through the blood, but the occurrence of caseous pneu- 
monia rather than miliary tuberculosis in such cases is assuredly 
rare. 

Mixed infection with Diplococci pneumonia? is not infrequent, 
but it is not, as some investigators have maintained, essential to 
the disease. 

Pathologic Anatomy. — In its most typical form caseous 
pneumonia is a lobular process beginning around the terminal 
ends of the bronchioles, where the infective material lodges. The 
lung presents on section areas of consolidation not unlike those 
seen in catarrhal bronchopneumonia. At first these are congested 
and red in color, but very soon degenerative changes cause a 
grayish or yellowish color. The surface of section is usually 
smooth, but often somewhat granular from associated fibrinous 
exudation. When abundant infection has occurred the areas may 
be thickly set, and a lobar form is thus established (Plate 6) ; or 



452 



TEXT-BOOK OF PATHOLOGY. 



there may be a gradual involvement of new areas, receiving their 
infection from those first formed, with a similar, but less uniform, 
lobar pneumonia as the result. 

Caseous pneumonia shows no tendency to resolution, but, on 
the contrary, tends to progressive cheesy degeneration, and at last 
to the formation of cavities. The entire lung may be riddled with 
small excavations, presenting ragged, cheesy walls. Usually the 
cavities are small, even though there be few ; exceptionally, large 
ones are seen. Though resolution does not occur, limited areas 
may be healed by reactive fibrous overgrowth springing from the 
alveolar septa and encapsulating the diseased area, or penetrating 
it, and transforming the whole into a fibrous mass. 

Microscopically the exudation has many of the characters seen 
in catarrhal bronchopneumonia. Essentially the exudate is cellu- 




Fig. 209.— Peribronchial tubercle of the lung and caseous pneumonia of the adjacent 

alveoli. 

lar, and is principally composed of large epithelial cells. These 
are the desquamated and proliferated lining-cells of the alveoli. A 
smaller number of red blood-corpuscles and leukocytes is noted, 
but they are unessential. Sometimes a fibrinous network may 
be seen in the alveoli, but quite as often this is wholly wanting. 
The blood-vessels are engorged at first, and the septa are infiltrated 
with round cells and spindle-cells. The walls of the blood- 



Plate 6. 




Subacute caseous (tuberculous) pneumonia (Bollinger). 



DISEASES OF THE RESPIRATORY SYSTEM. 



453 



vessels themselves may be thickened by proliferation of the con- 
nective tissue. As the process advances, the cellular exudate and 
the alveolar walls as well undergo cheesy degeneration, and pre- 
sent a granular appearance under the microscope (Fig. 209). 

Associated I^esions. — Cases of typical caseous pneumonia, 
as above described, are rare ; as a rule, more specific tubercular 
lesions are associated. These may result subsequent to the pneu- 
monic process from the penetration of infective material into the 
lymphatics and its dissemination along these channels ; or the 
specific tubercles may antedate the associated caseous pneumonia. 
The smaller bronchi are commonly attacked, and tubercular 
bronchitis and peribronchitis tending to cheesy change result. The 
pleura may be covered with inflammatory exudation, or may pre- 
sent miliary tubercles over the area of disease. Associated pleural 
involvement is especially common between the lobes. The lym- 
phatic glands of the anterior mediastinum and around the bronchi 
are frequently enlarged, and may be cheesy in the later stages. 

Fibrous Pneumonia. 

Definition. — Fibrous, or productive, pneumonia is a chronic 
process resulting from continued irritation, and involving small or 
large areas of the pulmonary structure. Pathologically it is 
characterized by overgrowth of connective tissue, and clinically it 
is marked by signs of more or less extensive mechanical impair- 
ment of the pulmonary functions. 

Classification. — Several quite distinct forms, depending upon 
different modes of causation, may be described. The principal 
varieties are : (1) the pneumonokonioses, or fibrous pneumonias, 
due to dust-inhalation ; (2) the secondary indurative pneumonias, 
such as sometimes follow croupous, catarrhal, or caseous pneu- 
monia, or more frequently chronic congestion of the lungs or 
atelectasis ; (3) pleurogenetic fibrous pneumonia, in which the 
process arises by extension of chronic pleural disease ; and (4) 
peribronchial and perivascular fibrous pneumonia, in which the 
process follows the bronchi and pulmonary arteries. 

1. Pneumonokoniosis. — Of the dust we constantly inhale, but 
a small part reaches the finer divisions of the bronchial tree. 
Most of it adheres to the walls of the upper respiratory tract and 
is discharged with the sputa, either free or enclosed in leukocytes 
or epithelial cells (dust-cells; staubzellen). When fine particles 
reach the terminal bronchioles they occasion catarrhal inflamma- 
tion, marked by proliferation of the epithelium and exudation of 
leukocytes. These cells may envelop the irritant particles and 
remove them through the expectoration. When, however, the 
dust has sharp edges (as in coal-dust, iron-dust, marble-dust, etc.), 
and especially when the quantity inhaled is considerable, removal 



454 



TEXT-BOOK OF PATHOLOGY. 



by expectoration becomes more difficult. In such cases the foreign 
particles penetrate the walls of the bronchioles and alveoli, passing 
between the epithelial cells. They may be arrested in the alveolar 
septa and in the tissue surrounding the bronchioles by the for- 
mation of a zone of inflammatory exudation, which eventually 
organizes, forming a fibrous capsule. Some of the particles, how- 
ever, move along the lymph-spaces into the lymphatic vessels, 
being carried by leukocytes or floating free in the liquid. These 
particles may be arrested at various points along the lymphatics, 
and may occasion fibrous thickening of the vessels or of the peri- 
lymphatic tissue. The greater portion, however, passes to the 
lymphatic glands at the root of the lung and surrounding the 
bronchi, and indurative enlargement of these structures results. 
In exceptional instances the irritant particles may be conveyed 
still further, being deposited in the glands about the smaller curva- 
ture of the stomach and beneath the fissure of the liver. This 
unusual distribution in a direction opposite the usual lymphatic 
current is explained by the assumption that obstruction of the 
larger pulmonary lymphatics causes a reversal of the current. 
Metastatic distribution of dust-particles may also be due to 
rupture of one of the affected lymphatic glands into a vein. 

Pathologic Anatomy. — The appearance of the lung varies with 
the amount of dust inhaled and with its nature. In cases of 
moderate degree small areas of fibrous thickening, with puckering, 
are the only abnormality. On section these are found to be hard 
and of grayish color ; often, however, darkly pigmented, owing to 
the character of the particles inhaled as well as on aceount of the 
formation of hemorrhagic pigmentation. The fibrous tissue may 
be arranged in a stellate fashion, or concentrically around a nucleus 
of foreign matter. Secondary changes are not uncommon ; calci- 
fication is frequently observed, and true bone-formation is occa- 
sionally noted. Such areas of localized pneumonokoniosis are 
very commonly met with near the apices. 

More extensive induration is rare, and is rather more frequent 
at the bases. Large areas of induration may completely de- 
stroy the vesicular character of the lung-structure. Firm bands 
of connective tissue may follow the bronchi and radiate into the 
peripheral portions of the lung, or thickened trabecular may pass 
from the pleural surface toward the anterior, or, again, a more 
uniform sclerosis may exist throughout the organ. The organ is 
contracted ; the pleura, as a rule, is thickened and drawn inward ; 
and the bronchi may be widely dilated as a result of the traction 
of the contracting connective tissue and as a consequence of accumu- 
lating secretions within. Extensive adhesions to the chest-wall 
often cause deformities of the chest, and the pericardium, heart, 
and other mediastinal structures may be drawn from their normal 
positions. 



DISEASES OF THE RESPIRATORY SYSTEM. 



455 



In rare cases the epithelium of the alveoli and finer bronchioles 
proliferates, and later undergoes a certain amount of fatty degen- 
eration, giving rise to an appearance not unlike caseation. In still 
other cases necrosis and suppuration and cavities (non-tubercular) 
are observed. 

Microscopically. — In the beginning stages round-cell infiltration 
and connective-tissue proliferation may be seen around the foreign 
particles in the septa, and a certain amount of catarrhal inflam- 
mation may be present in the alveoli. Sharp-edged particles often 
occasion small hemorrhages. In the later stages dense sclerotic 
tissue characterizes the process. Proliferative inflammation of the 
epithelium of the alveoli may be present, but more often the cells 
undergo atrophy and disappear. 

Varieties. — Certain varieties, dependent upon the kind of dust 
inhaled, have been described. The term anthracosis is applied to 
those instances in which coal-dust is the irritant. To a moderate 
extent this is seen at every autopsy on persons of adult age, but 
the cases in which conspicuous sclerosis has occurred from this 
cause are met with only in coal-miners and others of similar occu- 
pation. The lung is of a marble-like or slate-like appearance, and 
the lymphatic glands around the bronchi are intensely pigmented. 
Siderosis is the designation of the cases of pneumonokoniosis due 
to iron-dust, as seen in grinders, founders, etc. Chalicosis is the 
term applied to the form due to stone-dust, as seen in potters, 
marble-cutters, etc. 

2. Secondary fibrous pneumonia sometimes occurs after croup- 
ous or catarrhal pneumonia, or atelectasis, and in these cases 
appears in the form of uniform or localized induration of the pul- 
monary structure. It is due to reactive inflammation of the septa, 
causing thickening of the latter, as well as proliferation within the 
alveolar exudate. Similar reactive fibrous change is seen in some 
cases of caseous pneumonia, and in chronic phthisis the cavities 
are quite generally walled by fibrous tissue. Finally, chronic 
congestion of the lung, such as occurs in valvular diseases of the 
heart, particularly mitral disease, frequently leads to diffuse 
sclerosis of the lung. Such cases are distinguished by dilatation 
of the veins and by hemorrhagic pigmentation. 

3. Pleurogenic fibrous pueumonia is an occasional consequence 
of chronic pleurisy. ,The lung presents on section dense tra- 
becule of fibrous tissue, which extend from the thickened and 
sclerotic pleura deep into the pulmonary structure (Fig. 210). 

4. Peribronchial and perivascular fibrous pneumonia may be 
associated with the pleurogenic form, or the overgrowth of con- 
nective tissue around the bronchi and vessels may start at the 
root of the lung and extend toward the periphery. The latter 
form has been described by some observers as especially liable to 
result from syphilis. More moderate peribronchial and perivas- 



456 



TEXT-BOOK OF PATHOLOGY. 



cular fibrous pneumonia occurs in association with other forms, as 
the pneumonokonioses and secondary fibrous pneumonias, but in 
these cases it is but a minor part of the process. 




Fig. 210.— Fibrous pneumonia secondary to chronic pleurisy (Kaufmann). 

Congenital Syphilitic Pneumonia. — A form of productive pneumonia, 
as distinguished from fibrous pneumonia in the strict sense that the latter 
is characterized by formation of sclerotic fibrous tissue, is met with in con- 
genital syphilis. This is the pneumonia alba of some writers. It is charac- 
terized by great proliferation of round and irregular connective-tissue cells, 
with more or less multiplication and degeneration of epithelial cells in the 
alveoli and bronchioles. The lung is solid, airless, and white in color. 
Gummata may be associated. 

Purulent Pneumonia. 

Definition. — Purulent pneumonia is an acute form of pneu- 
monia caused by pyogenic micro-organisms. Pathologically it is 
characterized by purulent and hemorrhagic exudation in the con- 
nective tissue, lymphatic channels, or terminal bronchioles and 
alveoli ; and clinically it is marked by evidences of intense septic 
infection as well as of great pulmonary embarrassment. 

The infection in purulent pneumonia may reach the lungs 
through the bronchi (bronchogenic), the blood-vessels (hemato- 
genic), or the subpleural lymphatics (pleurogenic or lymphogenic). 

Bronchogenic purulent pneumonia has already been referred 
to in the description of fibrinous pneumonia and catarrhal bron- 
chopneumonia. It is particularly frequent in the latter, in some 
cases of which considerable purulent exudation may be seen in 
the alveoli or, in the form of small purulent collections, in the 



DISEASES OF THE RESPIRATORY SYSTEM. 



457 



intervesicular septa. These are instances of intense infection, and 
the majority of such cases are due to the Streptococcus pyogenes 
or to staphylococci. The pneumococcus may, however, be found 
alone. The most decided purulent bronchopneumonia is seen in 
instances of aspiration-pneumonia secondary to a suppurative proc- 
ess in the upper respiratory passages, in which particles of infec- 
tive material are inspired and lodge in the bronchioles. 

Purulent pneumonia is rarely met in the course of fibrinous 
pneumonia, but sometimes occurs as a terminal condition. Ab- 
scesses of considerable size may be formed. 

Hematogenic purulent pneumonia is secondary to suppurative 
or gangrenous processes in other parts of the body, and is a 
manifestation of pyemic infection. It is frequent in puerperal 
septicemia, in suppurative osteomyelitis, and like conditions. 
The micro-organisms are carried by the veins to the right heart, 
and may first set up malignant endocarditis, from which embolism 
takes place, or they may pass directly through the right heart to 
the lungs. As a rule the micro-organisms in question are either 
streptococci or staphylococci ; but in certain specific infections 
(as typhoid fever) the specific organisms may alone occasion puru- 
lent pneumonia. 

When large embolic masses reach the lungs occlusion of larger 
branches of the pulmonary artery occurs and hemorrhagic infarcts 
are formed. In the earliest stages these appear as more or less 
well-circumscribed areas of hemorrhagic infiltration of dark-red 
color. Very soon change of color occurs, and the foci alter to a 
grayish, then a yellowish, color, and finally liquefy, forming sup- 
purative cavities, with irregular walls. The tissue around is in- 
tensely engorged and edematous, and not rarely quite hemorrhagic. 
Microscopically it presents the appearances of a catarrhal and 
hemorrhagic pneumonia. The abscesses frequently break into the 
bronchi and discharge their contents ; more rarely rupture into 
the pleural sacs occurs. The pleura itself is intensely inflamed 
over the embolic areas, and, as a rule, is covered with fibrino- 
purulent exudate. Extensive purulent pleurisy {empyema) may 
occur. 

When the micro-organisms reach the lung in a more dissemi- 
nated manner they pass at once to the smaller arterioles and capil- 
laries. Embolic infarcts are wanting in such cases, but there is 
diffuse serous, hemorrhagic, catarrhal, and purulent exudation, 
which causes consolidation of a somewhat gelatinous character. 
Small foci of suppuration may be seen, and the purulent process 
may visibly extend to neighboring parts of the lung along the 
lymphatic vessels. 

Terminations. — In either of the above forms, the localized 
embolic or the diffuse, necrosis or gangrene of the pulmonary tissue 
may occur. Occasionally recovery takes place by absorption of 



458 



TEXT-BOOK OF PATHOLOGY. 



the purulent exudate or by its discharge. As a rule, the disease 
is fatal. 

Pleurogenic purulent pneumonia follows intense pleurisy, usu- 
ally of purulent type. Infection of the subpleural lymphatics 
first ensues, and later the purulent process extends into the lung 
within and around these vessels {purulent lymphangitis and peri- 
lymphangitis), in the form of yellowish streaks or bands, which 
surround the veins and bronchi and follow the interlobular fibrous 
tissue in various directions. The lobules of the lung may be so 
pushed apart that the term pneumonia desiccans is quite applicable. 
The proper substance of the lung adjoining the paths of purulent 
invasion, and under the pleura, frequently shows the same form of 
hemorrhagic and purulent pneumonia as occurs in the diffuse 
hematogeuic form. 

Associated Lesions. — Widespread pyemic and toxic lesions 
are often found in association with purulent pneumonia, but they 
are often merely coincident results of the same primary disease 
to which the pneumonia owed its origin, rather than the conse- 
quences of the purulent pneumonia itself. Secondary infections 
may, however, occur, such as malignant endocarditis of the left 
side of the heart, septic nephritis, and the like. 

GANGRENE. 

Gangrene of the lung results from the action of putrefactive 
micro-organisms in necrotic areas of the lung-tissue. It may be 
the consequence of direct extension of carious conditions of the 
ribs or other adjacent bony structures through the pleura into the 
lung, or of the extension of necrotic processes from ulcers or can- 
cerous disease of the esophagus or stomach. In other cases the 
infective materials reach the lung through the inspired air, coming 
from ulcerative processes in the upper air-passages, or from with- 
out. When foreign bodies lodge in the bronchi, or the latter are 
obstructed by the pressure of tumors or aneurysms, there may be, 
first, more or less congestion and pneumonic consolidation, follo wed 
by secondary infection and gangrene. In still other instances the 
infective material reaches the lung through the blood, and, finally, 
gangrene is sometimes a terminal process in pneumonia, tubercu- 
losis, and hemorrhagic infarction of the lungs. Certain general 
conditions predispose more or less to it. Thus in diabetic indi- 
viduals congestions or pneumonia are prone to terminate in this 
way, and engorgement of the veins or passive hyperemia always 
renders the lung more liable. 

Pathologic Anatomy. — Gangrene may appear as a circum- 
scribed or diffuse process. In the former instances more or less 
extensive areas of lung present a dark, reddish, brownish, or even 
greenish appearance, and are surrounded by a zone of intense con- 



DISEASES OF THE RESPIRATORY SYSTEM. 



459 



gestion or of pneumonic consolidation, often of purulent or hemor- 
rhagic type. The diseased part is soft, pultaceous, and foul in 
odor. Later it may break down into a putrid mass, and may dis- 
charge through the bronchial tubes, severe pulmonary hemorrhages 
sometimes occurring at the same time. The bronchi and the 
blood-vessels often escape the process, and may pass through the 
gangrenous area without being themselves materially affected ; 
but usually the bronchi are penetrated, and the blood-vessels, after 
they become occluded by thrombosis, suffer the fate of the other 
tissues. The process may extend widely from a single focus, or 
reactive inflammation may establish a fibrous capsule, and after 
discharge of the gangrenous material through the bronchi, healing 
by the formation of a scar may terminate the disease. 

Diffuse gangrene does not differ much in its general appear- 
ances, but is less intense and in general more widespread. The 
affected area is of a dark-red or greenish-black color, soft, and edem- 
atous, or sometimes dry, and has a somewhat fetid odor, as in 
the circumscribed form. Spots of hemorrhagic infiltration and of 
softening, with formation of cavities, may be noted. 

The sputa in gangrene are mucopurulent, of a yellowish-gray 
or brownish color, and intensely fetid. When placed in a conical 
vessel they separate into three layers : the upper frothy, the lower 
puriform and brownish in color, and the middle layer more fluid 
and yellowish. 

INFECTIOUS DISEASES. 
Tuberculosis. 

Tuberculosis of the lungs is generally a local disease, but 
may be only part of a general tuberculosis. The specific cause, 
the tubercle-bacillus, gains access to the lungs through the same 
channels as the irritants that occasion pneumonia. The most fre- 
quent method of infection is through the air-passages (broncho- 
genic tuberculosis), the bacilli in such cases coming directly from 
the outside world or from a tuberculous lesion of the nose, mouth, 
pharynx, larynx, or bronchi. The latter lesions in turn are fre- 
quently caused by bacilli inhaled from without, the bacilli owing 
their presence in the inspired air to the desiccation and dis- 
semination of sputa of phthisical patients (see Tuberculosis, in 
Part L). A second method of infection is that through the 
blood (hematogenic tuberculosis). The pulmonary disease in 
such cases is usually secondary to a tuberculous lesion elsewhere 
which has perforated a vein and discharged its contents into the 
blood. In such cases general tuberculosis results, and the lungs 
are affected in common with other vulnerable structures. The 
infected material may reach the blood in a more roundabout way, 
when a tuberculous gland or other focus breaks into a lymphatic 



460 



TEXT-BOOK OF PATHOLOGY. 



vessel (commonly the thoracic ducts in cases of tuberculosis of the 
abdominal or posterior thoracic lymphatic glands). Hematogenic 
tuberculosis may in rare instances be limited to the lung, and be 
secondary to an older tuberculous lesion of the lung itself. This 
happens when a caseating nodule perforates a branch of the pul- 
monary artery and the infective matter is carried to the peripheral 
distribution of the artery. The third and last method of impli- 
cation of the lungs is through the lymphatic vessels (lymphogenic 
tuberculosis). This may be secondary to tuberculous pleurisy or to 
caseous tuberculosis of the peribronchial lymphatic glands or of 
the thoracic vertebrae. 

Bronchogenic Tuberculosis. 

The action of the tubercle-bacillus when inhaled may be likened 
to the action of dusi>particles entering the lungs in a similar 
manner. Larger masses of infective material may lodge in the 
bronchi or larger bronchioles and set up tuberculous ulcerations, 
from which smaller particles may be secondarily aspirated into the 
finer divisions of the bronchial tree. Such an occurrence, how- 
ever, is extremely rare. More commonly the tubercle-bacilli are 
inhaled in a state of extreme dissemination, and are not arrested 
until they reach the point of division of the terminal bronchioles 
into the alveolar passages. One of two results may occur at 
this point : either there is set up a limited area (miliary nodule) 
of caseous or tuberculous pneumonia, or the bacillus penetrates 
between the epithelial cells and occasions more specific tubercular 
changes in the peri-alveolar and peribronchial connective tissues 
(miliary tubercles). It has been the occasion of some dispute 
among pathologists to decide which of these processes is most apt 
to arise when the infection occurs through the bronchial tubes. 
Undoubtedly both kinds of change may take place, and it seems 
likely that in nearly every instance there is a mixture of the two 
fjrms. When the infective material is in great abundance and is 
particularly virulent, and in cases in which the individual is 
especially vulnerable, caseous pneumonia predominates over the 
formation of tubercular nodules. On the other hand, a less 
abundant infection or greater resisting power on the part of the 
individual determines the greater liability to the formation of 
nodules and the less likelihood of extensive caseous pneumonia. 
In case of either manner of onset, however, there is soon added 
the other form of disease. Thus in the instances in which caseous 
pneumonia first occurs, the peribronchial involvement character- 
istic of that condition leads to dissemination of the bacilli along 
the lymphatic channels, and there are formed in the neighborhood, 
or to considerable distances around, miliary nodules, which in turn 
spread the infection to the alveolar structures in their vicinity. 



DISEASES OF THE RESPIRATORY SYSTEM. 461 



In a similar manner, when the primary lesion is a tubercular 
nodule surrounding the alveolar passages, the alveoli soon be- 
come involved by caseous pneumonia. 

At the same time that these processes are taking place and 
spreading, degenerative and reparative changes are set on foot. 
The areas of pneumonia, which began as grayish miliary nodules or 
as larger areas of lobular tuberculous pneumonia, change their color 
to a yellowish and become completely caseated ; while the second- 
ary tubercles in the neighborhood, or those which were primarily 
formed, similarly become opaque and lusterless, and finally yellow- 
ish by caseation. This tendency to caseous necrosis is one of the. 
most prominent and characteristic features of tuberculous tissues, 
and has occasioned no little investigation and controversy to 
establish its causation. Little doubt now exists that two factors 
play a part : first, the lack of adequate blood-supply, and, second, 
the specific action of the tubercle-bacillus. The blood-vessels in 
caseous pneumonia or in the tubercles are inadequate to supply 
sufficient nourishment to the tissue. In the pneumonic areas this 
is due to proliferative changes in the intima and to direct pressure 
of the exudate, while in the tubercles it is due to hyaline and 
other forms of degeneration with collapse of the walls. 

Coincidently with the process just described round-cell infil- 
tration and proliferative changes are manifest in the structures 
surrounding the diseased areas. In the case of the areas of caseous 
pneumonia infiltration and proliferation of the connective tissue of 
the septa, as well as proliferative changes in the blood-vessels of 
these parts, are observed. There is a w T ide variation in particular 
instances in the degree of these reparative processes, and in gen- 
eral it may be said that the more acute the disease the more apt 
is degenerative caseation to take place and the less likely regener- 
ation to occur. Similar overgrowth and infiltration may be seen 
around the tubercles, and in favorable instances the latter may be 
completely encapsulated or converted into a fibrous nodule. In 
instances in which the reparative processes are very extensive 
there may eventually be a preponderance of connective tissue over 
caseous pneumonia or miliary tubercles. 

Varieties. — We may distinguish all of the forms of broncho- 
genic tuberculosis by the name of pneumonic tuberculosis, from the 
fact that the element of caseous pneumonia is always an important 
one, and separates them sharply from hematogenic and lympho- 
genic tuberculosis, in both of which the formation of miliary 
tubercles predominates over other processes. 

Three forms of pneumonic tuberculosis are met with : the 
acute, which is frequently spoken of as acute caseous phthisis, or 
galloping consumption; the chronic, Avhich is also known as 
chronic ulcerative phthisis ; and the form in which fibrous over- 
growth predominates, and which is therefore known as fibrous or 



462 



TEXT-BOOK OF PATHOLOGY. 



fibroid phthisis. While typical instances of these forms are quite 
distinct, there is no sharp dividing-line separating the groups, and 
individual forms merge insensibly one into the other. 

Acute pneumonic tuberculosis is more common in children than 
in adults. Two elements play a part in its occurrence : first, a 
high degree of susceptibility, and, second, abundant infection with 
virulent bacilli. The latter may be derived from without the body 
by direct inhalation, or may come from the discharge of older 
caseous areas in the lungs, which have broken into the bronchial 
tubes, or from some focus of tuberculosis in the upper air-pas- 
sages. 

Pathologic Anatomy. — This form of tuberculosis is lobular, 
but very frequently by confluence of the affected areas an entire 
lobe may be involved. Either the base or the apex may be first 
affected. On section the lung presents a more or less variegated 
appearance in the earlier stages, due to the formation of miliary 
patches and lobular areas of caseous pneumonia having a grayish 
appearance, and the coincident congestion of surrounding portions 
of the lung-tissue. Sections through the lung which cut a termi- 
nal bronchiole in a longitudinal direction show it surrounded by 
peribronchial caseation and more or less filled with cheesy exudate 




Fig. 211.— Bronchogenic tuberculosis of the lung, showing the involvement of the tissues 
surrounding the terminal bronchioles (Birch-Hirschfeld). 

(Fig. 211). Transverse sections give the appearance of a section 
through a large tubercle, but the lumen of the bronchiole may 
usually be discovered in the center or to one or the other side. 
Small miliary tubercles may be apparent in the edges of the pneu- 
monic patches, and even for some distance around them, but the 
tuberculous tissue is more apt to appear as diffuse infiltration along 
the peribronchial and perivascular lymphatics than as distinct 
tubercles. As the process increases the lung-tissue may be com- 
pletely involved and uniformly gray or yellowish and consolidated 



DISEASES OF THE RESPIRATORY SYSTEM. 



463 



(Fig. 212). The cut section is generally somewhat granular in the 
earlier stages from admixture of fibrinous exudation in the alveoli ; 
but later progressively increasing caseation and softening render 
the surface of section smooth 
and moist. Not infrequently 
complete destruction takes 
place and cavities are formed. 
These are usually small and 
present no marked tendency 
to the formation of an organ- 
ized wall, but appear simply 
as necrotic excavations with 
irregular, ragged outlines. The 
pleura over the surface of such 
a lung is usually inflamed and 
covered with more or less fibri- 
nous or fibrinopurulent exuda- 
tion, and not rarely with an 
abundant crop of tubercles. 
Occasionally a vomica may 
rupture and cause pneumo- 
thorax or pyopneumothorax. 

When the process is less 
active and the infection less 
abundant confluence of the 
lobular areas is less likely to 
occur, and there are seen 
merely disseminated patches 
of caseous pneumonia scat- 
tered through various parts 
of the lung, which is itself 
more or less congested. In 
such instances, too, the evi- 
dences of reparative change 
are more decided. Complete encapsulation with subsequent calci- 
fication may ensue, or fibrous overgrowth may convert the entire 
area into a cicatricial mass. If the cheesy area is simply enclosed 
with fibrous tissue, it may remain quiescent for a time, possibly 
for years, and subsequently penetrate the enclosing wall and occa- 
sion a fresh extension of the whole process. 

Chronic pneumonic tuberculosis is the ordinary form of pulmo- 
nary phthisis. It begins in the apices of the lungs in the great 
majority of cases, though children are as likely to be first affected 
at the bases as at the apices. While there is no doubt that chronic 
phthisis is usually due to infection through the inspired air, it 
must be admitted that occasionally the onset of the process is due 
to infection through the blood or lymphatic channels. In the in- 




Fig. 212.— Extensive bronchogenic tuber- 
culosis (caseous pneumonia) of the base of 
the lung (Orth). 



464 



TEXT-BOOK OF PATHOLOGY. 



stances of the latter kind there is first established a localized 
lesion which caseates and penetrates a bronchial tube, discharging 
its contents, and thus leading to widespread bronchogenic infec- 
tion. The further development of the disease takes place in sev- 
eral distinct ways (see below). 

Pathologic Anatomy. — When there has been an existing bron- 
chitis, adhesion of the bacilli may occasion tuberculous bronchitis 
with ulceration and secondary involvement of the surrounding tis- 
sues. More commonly the bacilli lodge in the finer bronchioles, as 
in acute pneumonic phthisis, and give rise to lobular areas of caseous 
pneumonia, surrounded by tubercles which are formed along the 
course of the lymphatic vessels leading out from the first-formed 
caseous areas. There is a tendency to a constant increase of the 
area of disease by the discharge of caseous material into the 
bronchi and its aspiration into other parts of the lung, and also 
by dissemination of the infection along the lymphatic vessels 
traversing the connective tissue around the blood-vessels and 
bronchi. Section through the lung discloses more or less consoli- 
dated tissue of an opaque, grayish or yellowish appearance, in 
which the bronchi may be seen as open spaces or filled with muco- 
purulent liquid. Little distinction between caseous pneumonia 
and the tubercles can be made in the center of such an area, but 
at the edges, where the process is seen in the earlier stages, such 
distinction may be possible. 

At times areas of a serofibrinous or gelatinous pneumonia are 
formed. These differ from caseous pneumonia in presenting a 
gelatinous appearance, and in their liability to partial or complete 
resolution. The process is serofibrinous and cellular in character. 

The same tendencies to degeneration and softening, on the one 
hand, and to the processes of repair, on the other hand, are seen 
in chronic pneumonic phthisis as are apparent in the acute form. 
There is the difference, however, that these changes are less rapid, 
and that, as a rule, proliferation of connective tissue with the for- 
mation of fibrous tissue is more pronounced than in the acute 
disease. 

The degenerative and necrotic processes lead to a most charac- 
teristic lesion of tuberculous lungs — the cavity. Cavities are formed 
either through the dilatation of the bronchioles (bronchiectasis), 
due to their ulcerated and weakened condition and to the pressure 
of retained secretions, with subsequent ulceration and break- 
ing down of the surrounding caseous tissue ; or, on the other 
hand, to liquefaction of caseous areas not in connection with the 
bronchial tube. In the latter case, hoAvever, communication with 
the bronchi is frequently established by extension. A single 
cavity may grow larger and larger by constant ulcerative proc- 
esses, in which not alone the caseous tuberculous degeneration 
takes a part, but also active ulcerative changes dependent upon 
mixed infection through inspiration of pyogenic organisms. As a 



DISEASES OF THE RESPIRATORY SYSTEM. 



465 



rule, however, larger cavities are formed by the confluence of 
separate smaller ones, and there may be found a series of ex- 
cavations communicating more or less extensively with each 
other. The cavity, or vomica, contains a variable amount of 
ill-smelling, putrid secretion, consisting of broken-down cheesy 
matter, pus-cells, degenerated epithelial cells, and iibers of elastic 
tissue, and containing tubercle-bacilli, pyogenic organisms, and 
occasionally mould-fungi. The walls of the cavity are generally 
formed by reparative fibrous proliferation, and are covered with 
a pyogenic membrane, usually darkly pigmented. The inner 
surface is very rough and ribbed by projecting bands. The latter 
represent the trabecular and blood-vessels of the lung-tissue, which 
have resisted ulceration more obstinately than the surrounding 
structure of the lung. This resistance may continue to such an 
extent that the blood-vessel is left as a cord passing directly 
through the center of the cavity ; but, as a rule, the lumen of 
the vessel is soon obliterated by thrombosis and the vessel itself 
destroyed. Not infrequently examination of the blood-vessels in 
the wall of the cavity or passing through it show small aneurysmal 
dilatations which result from the weakening of the wall by the 
surrounding necrotic process and from the pressure of the blood 
within. It is from aneurysms of this character that the large and 
often fatal hemorrhages of the later stages of tuberculosis take 
place, though hemorrhage may also occur directly from the eroded 
blood-vessel. The smaller hemorrhages of the early stages of 
phthisis, which occasion only a streaking of the sputa with blood, 
are due to early erosion of small vessels of the bronchioles or to 
capillary ruptures dependent upon congestion. 

Fibroid Phthisis. — The reparative or fibrous processes which 
tend to counteract caseation and destruction may begin before 
cavity-formation or after it. When beginning in the earlier stages 
the caseous areas will be found to present a capsule of more or less 
well-developed fibrous tissue, which may completely surround and 
separate them from the neighboring tissue of the lung. The cap- 
sule tends to contract and shrink, and the caseous material within 
may become completely calcareous. In this manner a limited 
focus of tuberculosis of the lungs not infrequently becomes com- 
pletely arrested. When the capsule is not so firm, after a period 
of quiescence or latency extending over even a number of years, 
fresh extension may begin, the capsule may be perforated, and 
acute pneumonic phthisis may be established, or the tubercu- 
lous process may extend more slowly through the contiguous areas 
as chronic ulcerative phthisis. 

The fibrous capsules surrounding the cavities, which have 
already been alluded to, may be of varying prominence. In case 
of small vomicae with pronounced fibrous walls the contraction of 
the latter may almost obliterate the cavities, leaving only narrow 
and distorted spaces containing a small amount of putrid material 

30 



466 



TEXT-BOOK OF PATHOLOGY. 



{cicatrices fistuleuse of Laennec). Complete healing of a cavity 
of notable size probably never occurs. When the excava- 
tions are of large size the reparative processes consist simply 
in the formation of a thick wall of fibrous tissue, which prevents 
the further extension, for a time, at least, of the tuberculous 
process. 

Complications in Bronchogenic Pneumonia. — Of first im- 
portance in tuberculosis of the lung is the condition of the pleura. 
In the acute pneumonic form the pleura adjoining the diseased 
areas is generally more or less inflamed and may present consider- 
able fibrinopurulent exudation, as in croupous pneumonia. Serous 
or seropurulent exudation may likewise be present, and eruption 
of miliary tubercles in the pleura is not unusual. The same proc- 
esses may occur in chronic pneumonic tuberculosis or chronic 
phthisis. More commonly there are found simply fibrous adhe- 
sions binding the one surface of the pleura to the other, especially 
at the apex. 

Extension of the tuberculous process may also take piece 
directly upward along the air-passages, and is due for the most 
part to direct infection by the sputa. There may thus occur tube r- 
culous ulceration of the larger bronchi, of the trachea, of the 
larynx, or of the pharynx. When the sputa are swallowed, as is 
especially likely to happen in children, or in adults during sleep, 
intestinal tuberculosis is apt to occur. 

Finally, dissemination of the tuberculous disease through the 
blood is frequent. A caseous area in connection with one of the 
veins may penetrate the lumen of the vessel and discharge its 
contents into the circulating blood, or may first occasion tuber- 
culous proliferation in the intima of the vein or infectious throm- 
bosis, from which the blood is secondarily infected. There results 
general miliary tuberculosis, the tubercles ' occurring especially in 
the spleen, the liver, the kidneys, the choroid coat of the eye, or in 
the membranes of the brain or other serous membranes. 

Acute pneumonia may accompany either acute or chronic pneu- 
monic tuberculosis, and certain authors insist that in practically all 
cases there is more or less mixed infection. This is probably not 
the case, but complicating pneumonia is undoubtedly frequent. 
In most of such cases localized patches of catarrhal bronchopneu- 
monia are seen between the caseous lobules ; but sometimes a frank 
fibrinous consolidation may occupy the lower lobe of a lung in 
which the upper lobe presents beginning tuberculosis. Quite fre- 
quently there are small areas of pneumonic consolidation of fibri- 
nous character in the lobe which is itself the seat of tuberculous 
involvement. Toward the end of life there is usually extensive 
edema of the bases and posterior portions of the lungs. 

The heart has interesting relations with tuberculosis of the 
lungs. Early writers called attention especially to the fact that 
phthisical subjects frequently present unusual smallness (hypo- 



DISEASES OF THE CIRCULATORY SYSTEM. 467 



plasia) of this organ, and more recently attention has been directed 
to the fact that congenital stenosis of the pulmonary orifice strongly 
predisposes to tuberculosis of the lungs. Some have claimed that 
there is an antagonism between cardiac disease and tuberculosis. 
This view is not well founded, though it is probable that the 
chronic congestion of cardiac disease renders the lung somewhat 
less vulnerable to tuberculous infection than the normal lung. 
Where there is a long-standing tuberculous consolidation hyper- 
trophy, especially of the right ventricle, is likely to occur. Tuber- 
culous pericarditis may be found in association with tuberculous 
pleurisy ; and tubercles may also, though much more rarely, be 
found upon the endocardial lining. The latter are due to infec- 
tion through the blood. 

Hematogenic Tuberculosis. 

This form occurs when a focus of tuberculous disease ruptures 
into a blood-vessel and the infective materials are disseminated in 
the circulation. As a rule, hematogenic tuberculosis of the lungs 
is only a part of a general tuberculosis of the entire body. The 
points from which the primary infection may take place are, of 
course, numerous, but caseous lymph-glands of the cervical or 
peribronchial group, or old foci of tuberculosis at the apex of the 
lung, are perhaps the most frequent. The organs and structures 
of the body likely to be infected by general miliary tuberculosis 
are the spleen, the liver, the kidney, the choroid coat of the eye, 
the meninges, and, more prominently than any other organ, the 
lungs. In the rare cases in which rupture of the vomica has 
occurred into one of the branches of the pulmonary artery within 
the lung, only one lung, or but a part of a lung, may be involved. 

Pathologic Anatomy. — The pathologic feature of import- 
ance in hematogenic tuberculosis is the formation of miliary tuber- 
cles. These appear as gray or translucent areas, the size of millet- 
seeds, around and involving the terminal arterioles or capillaries 
in the intervesicular septa. At first they may be so small that the 
naked eye scarcely discovers them, and they are so translucent that 
oblique light is necessary to make them appear to view. Later 
they increase in size and become more grayish and opaque. Micro- 
scopically there are the well-known characteristics of the miliary 
tubercle embedded in the perivascular connective tissue (see Tuber- 
culosis, Part I.). These tubercles, however, are prone to distin- 
guish themselves from the characteristic tubercles seen elsewhere 
by their more irregular outline and the more irregular arrangement 
of their component histologic elements. When the tuberculous 
process is particularly rapid and virulent giant-cells are few in 
number, and the tubercle is composed mainly of proliferated 
connective-tissue cells of the ordinary type, some epithelioidal 
cells, and round infiltration-cells, all of them more or less granu- 



468 TEXT-BOOK OF PATHOLOGY. 

lar, and the entire nodule surrounded by a zone of caseous, 
catarrhal, or even hemorrhagic pneumonia of the contiguous 
alveoli of the lung (Fig. 213). The tubercles are rarely seen 




Fig.- 213. — Miliary tuberculosis of the lung, showing two tubercles with degenerated cen- 
ters, and caseous pneumonia of the alveoli adjacent to the tubercles (Orth). 

in the stage of advanced necrosis, but this may take place in 
instances of a more chronic course in which the bacteria are 
admitted to the lungs slowly and perhaps in a state of lesser viru- 
lence than common. In those instances of what may be termed 
chronic miliary tuberculosis there may be a considerable amount of 
caseation of the tubercles, and the patches, as a rule, become decid- 
edly larger than in the ordinary acute form (Fig. 214). An expla- 
nation of this form of chronic miliary tuberculosis has been offered 
by certain authors, who hold that these are instances of infection 
through the thoracic duct and blood-vessels. The infective material 
enters the thoracic duct from caseous lymphatic glands in the ab- 
domen or thorax, and is discharged with the lymph into the veins 
in a gradual manner, only a little being allowed to pass at a time. 

The ordinary and typical acute miliary tuberculosis presents 
itself clinically as an acute infectious disease, running its course 
rapidly and causing early dissolution. The disease is rather a 
general toxemia than a local process, and toxemic changes may be 
present in various organs, such as occur in other infectious and 
toxemic diseases. The heart, liver, the kidneys, and, in general, 
the parenchymatous structures are prone to become degenerated, 
and when the febrile infection continues there may be extensive 



DISEASES OF THE RESPIRATORY SYSTEM. 469 

fatty degeneration. In addition to the eruption of miliary tuber- 
cles in other organs, to which allusion has already been made, 
there is also involvement of the pleura which belongs more prop- 




Fig. 214. — Hematogenic tuberculosis, showing many scattered miliary tubercles and 
several clusters (modified from Bollinger). 

erly to the pulmonary process itself, and is simply a continuation 
of the same infection which gave rise to the pulmonary involve- 
ment. 

Lymphogenic Tuberculosis. 

It is possible for tuberculous infection of the lungs to occur 
through the lymphatic channels in several ways. In speaking of 
acute miliary tuberculosis, particularly of the more gradual type, 
reference was made to the fact that infective material is sometimes 
carried by the thoracic duct from the lymphatic glands of the 
abdomen and posterior mediastinum, as well as possibly from 
carious thoracic vertebrae to the blood-vessels, and thence distrib- 
uted through the blood to the lungs as a hematogenic infection. 
Direct infection, however, through the lymphatic channels may 
take place. Thus tuberculous pleuritis, either primary or second- 
ary to tuberculous disease of the vertebrae or ribs, sometimes 
spreads directly into the lung through the lymphatic vessels trav- 
ersing the interlobular connective tissue ; and in cases of caseous 
tuberculosis of the peribronchial glands the infective material may 
be conveyed into the lungs either by a reversal of the current of 



470 



TEXT-BOOK OF PATHOLOGY. 



lymph in the vessels running to these glands or by direct exten- 
sion along the lymphatic walls. A form of lymphogenic tuber- 
culosis of the lungs may also be referred to in which caseous 
lymph-glands directly perforate the lung-tissue, but the actual 
dissemination of the process in the lungs in these cases is usually 
through the bronchial tubes into which the bacilli gain entrance. 

Pathologic Anatomy. — It is characteristic of lymphogenic 
tuberculosis to find small nodular areas which microscopically are 
seen to be more or less characteristic tubercles. These are 
scattered along the lymphatic vessels running in the interlobular 
septa or surrounding the blood-vessels and bronchi. In the in- 
stances of lymphogenic tuberculosis secondary to pleuritis sup- 
purative lymphangitis and perilymphangitis (see Pneumonia) are 
not infrequently associated. 

SYPHILIS. 

It has been the occasion of much dispute whether the many 
forms of disease attributed to this cause can be really so classified. 
Undoubtedly some of the conditions attributed to syphilis are 
cases of tuberculosis, or of some other form of pulmonary disease. 
But there are other varieties which can unquestionably be spoken 
of as syphilitic. Among these are the diffuse infiltration of the 
new-born and the tertiary gummata. 

Diffuse syphilitic infiltration of the lungs is occasion- 
ally met with in the new-born. As a rule, infants showing this 
are stillborn. It manifests itself as a more or less lobar consoli- 
dation and induration of the lung-tissue. On section the lung is 
light gray or almost white in color, and completely airless, so that 
the name pneumonia alba, given by older writers, was highly 
significant. Microscopically there are seen widespread round- 
cell and spindle-cell infiltration and proliferation in the inter- 
alveolar and interlobular connective tissues, with more or less 
compression of the bronchioles and alveoli. The epithelium of 
the latter may be somewhat proliferated and desquamated, and 
shows a tendency to fatty degeneration and necrosis. In some 
instances the degenerative changes do not take place, and the 
proliferated epithelium of the alveoli is massed within the alveolar 
lumen, and is for the most part of a cuboidal character. The 
blood-vessels commonly show proliferation of the adventitia as 
well as of the intima, and may be completely obliterated. Ac- 
cording to Birch-Hi rschfeld, syphilitic fetuses of the sixth or 
seventh month sometimes present limited disease of this nature 
and of such distribution that it is recognized to begin as a peri- 
bronchial and peri-alveolar infiltration of lobular distribution. 

Syphilitic gTimmata may be associated with the diffuse 
form of congenital syphilis, or may be present in the new-born 



DISEASES OF THE RESPIRATORY SYSTEM. 471 

without the latter. Gummata are occasionally seen in adults. 
They are present most frequently near the root of the lung 
beneath the pleura, but may be scattered through other parts of 
the organ. As a rule, the number is limited. They appear as 
more or less rounded nodules of a grayish to yellowish color, with 
more or less fibrous overgrowth surrounding them and often 
radiating from them into the surrounding lung-tissue. Central 
necrosis may proceed to such extent that cavities are formed. 

Occasionally the contents of a gumma may be discharged 
through the bronchial tubes, or they may be absorbed and a 
cicatricial puckering of the lung-tissue may mark the place 
of the former disease. Microscopically there are seen in the 
earlier stages the ordinary appearances of gummata (see Syphilis, 
Part I.), with more or less diffuse infiltration surrounding them and 
with thickening and hyaline degeneration of the blood-vessels. 

Syphilitic fibrous induration of the lung, so-called, has 
been described, and it seems likely that some of the cases embraced 




Fig. 215. — Syphilis of lungs : a, thickened alveolar walls or stroma ; 5, partly longi- 
tudinal section of bronchus ; c, uninfiltrated alveoli ; d, new connective tissue infiltrated 
with small round cells ; e, cells lining alveoli ; /, artery showing thickened walls ; g, des- 
quamated lining cells (Linsley). 

in the description are really syphilitic in nature. The process 
begins, as a rule, at the root of the lungs, from which it radiates 



472 



TEXT-BOOK OF PATHOLOGY. 



through the tissue toward the pleura. The fibrous tissue, for the 
most part, surrounds the bronchi and blood-vessels (Fig. 215). In 
another group of cases the process spreads from the pleura and 
occasions the formation of dense bands of fibrous tissue passing 
inward into the lung-structure. In still other cases the fibroid 
overgrowth is so diffuse that the appearance presented resembles 
so closely that of pneumonokoniosis, that it is practically indis- 
tinguishable. It is quite probable that many instances, in which 
appearances such as these are met with, are not at all syphilitic ; 
but the occurrence of changes of this description in association 
with gummata, and, again, the occurrence of such changes without 
gummata in undoubtedly syphilitic individuals, make it likely that 
some at least are of this origin and nature. 

GLANDERS. 

Glanders occasionally affects the pulmonary tissue, the infec- 
tion taking place either by inhalation from ulcerated lesions in 
the nose or other portions of the upper air-passages, or more 
rarely by distribution of the bacilli through the blood. The lesions 
are of two kinds. There may be merely a grayish or purulent 
infiltration of a diffuse character, with the formation of abscesses 
and often with associated hemorrhagic infiltration. Considerable 
areas of the lung may be consolidated in this manner, or the 
process may be localized and lobular. In other cases nodular 
patches varying from the size of a hemp-seed to that of a pea are 
seen in various parts of the lung. These consist of masses of 
round cells, and show an early tendency to degeneration. More 
or less hemorrhagic and catarrhal inflammation of the alveoli 
surrounding these nodules may be present. 

ACTINOMYCOSIS. 

Actinomycosis is a rare affection of the lungs. It may result 
from the direct extension of actinomycosis of the lymphatic tissues 
and cellular structures in the anterior or posterior mediastinum, 
when there are formed in the pulmonary tissue fistulous necrotic 
tracts containing more or less cheesy and purulent material, in 
which the characteristic yellowish actinomycosis-granules are 
found. The latter on microscopic study show the actinomyces. 
The infection may also take place by a gradual descent of the 
process from the mouth or upper respiratory passages along the 
trachea and bronchi to the lung; or, more commonly still, by 
aspiration of the infective agents. In the latter cases nodules 
consisting of round cells are formed, and present themselves as 
grayish or grayish-red patches varying in size from that of a pea 
to that of a cherry, and showing a decided tendency to fatty de- 
generation and purulent softening. The surrounding lung-tissue 



DISEASES OF THE RESPIRATORY SYSTEM. 473 



is commonly consolidated, and presents the appearances of purulent 
and catarrhal or even hemorrhagic pneumonia. In many cases 
there is also a manifest tendency to productive changes, which lead 
eventually to the formation of more or less fibrous tissue within 
the alveoli and in the interalveolar and interlobular connective 
tissues. Not rarely this indurative process completely surrounds 
areas of degeneration and softening. 

TUMORS. 

The lungs are, comparatively speaking, a rare seat of tumors, 
though a variety of both primary and secondary growths occur. 

Connective-tissue Tumors. — Small nodular fibromata have 
occasionally been observed scattered through the lungs in the peri- 
bronchial connective tissue, and a few instances of similar nodules 
of lipoma are recorded. Chondroma is more common than either 
of these, and doubtless takes origin from the peribronchial carti- 
lages. Secondary chondromata have been observed in cases of 
chondroma elsewhere. True osteoma is rare, but more frequently 
ossification of sclerotic areas is met with in instances of pneumono- 
koniosis. 

Sarcoma is the most frequent connective-tissue tumor of the 
lungs. It may originate in the lymphatic glands surrounding the 
bronchi in the roots of the lungs, from the lymphatic nodes sur- 
rounding the smaller bronchi within the lungs, from the lymphatic 
vessels themselves, or from the subpleural or other connective 
tissue of the lung itself. Primary sarcoma is less common than 
secondary. In one form it presents itself as rounded masses of 
grayish or yellowish color lying around the bronchi in the root 
of the lung (Fig. 216). On section through this it is seen to con- 
sist of more or less enlarged and transformed lymphatic glands, 
and there may be secondary nodules scattered through the lung. 
This form of sarcoma is particularly common in pneumonokoniosis, 
as seen in the fibroid lungs of the cobalt-miners of Schneeberg. 
Primary sarcoma may also be of the form called endothelioma. The 
lymphatic vessels in the peribronchial tissue become filled with 
proliferated cells, and their ramification may be distinctly visible on 
section as a network traversing the pulmonary tissue. Primary sar- 
coma of the spindle-cell or round-cell variety may spring from the 
subpleural connective tissue. Giant-cell sarcoma has been observed. 

Secondary sarcoma is extremely common. It is seen in nearly 
all instances in which metastasis has occurred from a primary 
growth in any part of the body. In these cases there are found 
well-defined nodules of varying size, situated for the most part 
near the surface of the lung (Fig. 217). They are whitish in color 
and tend to soften. The lung-tissue between may be congested, 
and there may even be pneumonic consolidation. Secondary sar- 



474 



TEXT-BOOK OF PATHOLOGY. 



coma of the lung may also occur from direct extension of mediasti- 
nal sarcoma or of sarcoma in other of the surrounding structures. 
An interesting type of secondary sarcomatous involvement of the 
lungs occurs in what is termed malignant lymphoma or lymph- 
adenoma, either with or without leukemia, These may be consid- 
ered as instances of generalized lymphosarcoma. The lungs are 
found to contain small nodules, consisting of round cells embedded 
in a more or less reticular matrix of stellate and spindle-cells. 

Epithelial Tumors. — Carcinoma is practically the only form 
to be considered, though adenoma of the lung has been described. 
Carcinoma of the lung is certainly less frequent than was formerly 
believed, sarcoma having been confused with it, Massive cancer 
may start from the mucous glands of the larger bronchi near the 
root of the lung. The tumor is irregular, soft, and tends to ulcer- 




Fig. 216.— Lymphosarcoma of the post-bronchial glands, invading the lung; the lung is 
divided by a long incision and the halves laid open. 

ate in the center, forming cavities. Secondary nodules within the 
lung-tissue are seen along the lymphatic vessels surrounding the 
bronchi. Primary carcinoma may also start from the epithelium 
of the finer bronchial tubes. The proliferation soon penetrates the 
wall of the bronchus and extends along the lymphatic vessels in 
the peribronchial connective tissue. In this manner bands of new 
groAvth are seen traversing the lung. Occasionally squamous- 
celled carcinoma may originate in the epithelium of the terminal 
bronchioles and alveoli. 

Secondary carcinoma of the lungs is less frequent than second- 



DISEASES OF THE RESPIRATORY SYSTEM. 



475 



ary sarcoma. It may occur by metastasis from cancer elsewhere, 
and in these instances the appearance of the nodules is much the 
same as that of sarcoma. Secondary cancer of the lung may also 
result from extension of esophageal carcinoma or of cancer of the 




Fig. 217.— Secondary sarcomata of the lung: the primary growth was attached to the 

pleura. 

breast penetrating the thoracic walls and pleura. Finally, in car- 
cinoma of the upper respiratory passages or of the mouth inhalation 
of cancerous particles may lead to secondary nodules in the lungs, 
associated at times with areas of broncho-pneumonia. 

Cysts. — Congenital cysts have been described, but they are 
probably merely dilatations of the bronchi. Adenomatous pro- 
liferation of the epithelial lining of such dilatations may take place. 
Dermoid cysts are rarely encountered. They may discharge 
through the bronchial tubes. 

PARASITES. 

Besides the specific and pathogenic micro-organisms that have 
been referred to as occurring in tuberculosis, pneumonia, and 
other infectious diseases, various forms of bacteria and mould- 
fungi are met with as accidental and non-specific parasites. Such 



476 



TEXT-BOOK OF PATHOLOGY. 



micro-organismal collections are most frequent in areas of gan- 
grene, in degenerated infarcts, and in dilated bronchi or tubercular 
cavities. Sarcinse, a form of leptothrix resembling that seen so 
frequently in the mouth, and several varieties of aspergillus, have 
been noted. The general term Pneumonomycosis aspergillina is 
applied to the occurrence of the last-named mould-fungi in the 
lungs. Sometimes they are so abundant that they are readily dis- 
covered in the sputa ; and it is likely that certain inflammatory 
conditions of the lungs are directly due to such organisms. The 
clinical course may suggest tuberculosis, and pathologically diffuse 
or irregular consolidation of the lungs may characterize such cases. 

Animal Parasites. — Of the lowest forms of animal life or 
protozoa, the Monas lens, cercomonas, and paramecium have been 
observed. These are entirely accidental, occurring in cases of 
gangrene, putrid bronchitis, and similar conditions. The class of 
vermes furnishes the more important parasitic affections of the 
lungs. The Distoma pulmonale is not infrequent in parts of Asia. 
It occasions serious hemoptysis. The Strongylus longevaginatus, 
echinococcus-cysts, and Cysticercus celhrfosce are occasionally seen. 
Pentastomum denticulatum has been observed. 

THE PLEURA. 

Anatomic Considerations. — The pleura is a membrane 
composed of fibrillar connective tissue and elastic fibers, contain- 
ing a rather abundant network of capillaries. It is lined on the 
surface with a single layer of flat endothelial cells, between which 
there are openings from the pleural cavity into the subpleural 
lymphatics. The latter form a rich network in the subpleural 
connective tissue and play an important part in the pathologic 
processes affecting the pleura. 

CIRCULATORY DISTURBANCES. 

Passive hyperemia occurs in various diseases interfering 
with the respiration, and still more intensely in cases in which 
there is pressure upon the azygos veins or diffuse intrathoracic 
pressure. 

Petechial hemorrhages may occur when the congestion is 
intense. They are particularly frequent and prominent in cases 
of death from suffocation, but are also seen in various disorders 
of the blood and hemorrhagic diatheses, such as pernicious anemia, 
purpura, and intoxications of various kinds. 

Hemothorax is the term applied to the presence of free blood 
in the pleural cavity. It may be due to wounds of the chest-wall, 
causing rupture of blood-vessels, to fracture of the ribs, and to 
rupture of aneurysms into the pleural sac. If the pleura is in a 



DISEASES OF THE RESPIRATORY SYSTEM. 



477 



healthy condition and secondary infection does not take place, 
more or less rapid absorption of the blood ensues. When infec- 
tion occurs, secondary inflammations of the pleura and disorgani- 
zation of the blood result. 

Hydrothorax, or dropsy of the pleural cavity, may be but a 
part of a general edema occurring in chronic kidney-disease or 
heart-disease. It is usually bilateral, and the fluid presents the 
ordinary characteristics of a serous effusion. Unilateral hydro- 
thorax is, however, not infrequent in cardiac disease attended with 
great enlargement of the organ. The hydrothorax in such cases 
is generally right-sided, and is probably due to pressure upon the 
azygos veins and the root of the right lung. The pleura itself is 
not particularly disordered, but very frequently some opacity and 
loss of luster is noted, and there may be edema of the subpleural 
fibrous tissue. The lungs are pressed backward toward the root 
and against the spinal column, and may be considerably com- 
pressed. Unilateral hydrothorax may be due to pressure, upon the 
veins of one side by tumors or aneurysm. A small amount of 
serous outpouring into the pleural sacs occurs quite commonly just 
prior to death. 

Hydrothorax causes compression of the lungs and displacement 
of the other adjacent viscera. The seriousness of the results are 
in proportion to the amount of effusion. 

Pneumothorax designates the presence of air in the pleural 
cavities, It may result from rupture of tuberculous vomica?, gan- 
grenous areas, softened hemorrhagic infarcts, or abscesses of the 
lungs, or rupture of emphysematous air-vesicles beneath the pleura, 
allowing egress of air into the pleural sac. It may also occur after 
an empyema has ruptured into the lung and established a fistu- 
lous communication between the pleural sac and the bronchioles. 
Very rarely it is due to a penetrating wound of the chest. The 
pleural sac may be more or less tensely distended with air ; the 
lung is pushed backward against the spine, is more or less gray- 
ish or brownish in color, indurated and airless. The pleura 
itself may present no abnormality, and the air may be absorbed ; 
but very frequently infection takes place, and purulent exudation 
from the pleura collects in the sac. The condition is then spoken 
of as pyopneumothorax. The neighboring organs are often greatly 
displaced, particularly the heart, the diaphragm, and the liver. 
In left-sided pneumothorax the heart may be pushed far to the 
right of the sternum, and when the right side is affected the liver 
may be pushed downward considerably below the ribs. 

INFLAMMATION. 

Inflammation of the pleura, or pleuritis, is designated 
by the clinical name pleurisy. 



478 



TEXT-BOOK OF PATHOLOGY. 



Etiology. — It may result from local or from general causes. 
Among the local causes the most important are extension of inflam- 
mation from the lungs in the various forms of pneumonia, in gan- 
grene and tuberculosis ; extension from pericarditis or mediastinal 
diseases, and extension from inflammatory affections of the spine, 
of the ribs, or of the chest-walls. Less directly peritonitis, hepatic 
abscess, and other abdominal affections may occasion pleuritis by 
extension, and in rare cases perforation of esophageal or gas- 
tric ulcers, or abscess of the spleen or liver, may be the 
cause. 

In the group of cases due to general causes the pleural inflam- 
mation is the result of infection or intoxication involving the 
pleura through the blood. Thus in pyemia and septicemia, in rheu- 
matism, and in other acute infectious diseases, and in Bright's dis- 
ease, acute inflammation of the pleura is not uncommon. Cold 
and traumatism have long been regarded as important causes, but 
their action is doubtless only a predisposing one, the immediate 
cause being some infection for which the traumatism or the 
exposure to cold has paved the way. 

The micro-organisms found in pleurisy are quite numerous. In 
the cases secondary to ordinary pneumonia, pneumococci are fre- 
quently discovered, and these micro-organisms may be present 
even though there be no pneumonia at 'all. In the instances 
secondary to tuberculosis of the lungs, as well as sometimes 
in cases of primary pleurisy without affection of the lungs, 
tubercle-bacilli are discovered. In the purulent cases, as well as 
in some instances of simple fibrinous or serofibrinous pleurisy, 
staphylococci and streptococci are detected. When there is 
abundant liquid it is always difficult to discover the micro-organ- 
isms, and in many instances in which bacteria have not been found, 
it is probable that the difficulty of their demonstration, even by 
animal experimentation, accounts for the failure to demonstrate 
them, rather than their absence. A number of forms have occa- 
sionally been seen, such as the Bacillus coli communis, the typhoid 
bacillus, the bacillus of anthrax, and others. 

Pathologic Anatomy. — Several forms of pleuritis may be recog- 
nized, though one of these merges into the other, and a single case 
may pass from one into another form at its various stages. It is 
well, however, to separate these stages as distinct forms, since 
many cases maintain a uniform character throughout. The forms 
are the fibrinous, serofibrinous, 'purulent, and hemorrhagic ; after 
any of these forms there may be left chronic pleural thickening or 
adhesions of a fibroid character. 

Fibrinous pleuritis begins with congestion and loss of luster 
of the pleural surface, after which there soon follows exudation of 
a fibrinous character, forming a thin, whitish pellicle on the sur- 
face. This may become yellowish and increase in thickness, so 



DISEASES OF THE RESPIRATORY SYSTEM. 479 



that the pleural surfaces become agglutinated, and when separated 
present an appearance likened to the appearance of two pieces of 
buttered bread separated after having been pressed together 
{bread-and-butter pleurisy). This process may be confined to 
small areas of the pleura, or it may be quite universal. Some- 
times it is limited to the reflections of the pleura separating the 
lobes of the lung. 

Microscopically the exudate consists of fibrils or flakes or 
granular masses of fibrin more or less infiltrated with round cells. 
Beneath this the endothelium of the pleura is found to be some- 
what thickened by proliferation and some of the cells are detached. 
The connective tissue beneath the endothelium and the subpleural 
connective tissue are infiltrated with round cells and the blood- 
vessels are hyperemic. In favorable cases and when the process 
has been slight a gradual reabsorption of the exudate takes place, 
and the integrity of the pleura may be restored completely. 
When the exudate has been more extensive and the agglutina- 
tion of the pleural surfaces has been considerable, new blood- 
vessels from the capillaries of the pleura penetrate the fibrinous 
exudate, fibroblastic cells develop from the older connective-tissue 
cells, and gradually organization takes place, so that the adjacent 
layers of pleura are bound together by connective tissue, the 
fibrinous exudate gradually undergoing absorption and disappear- 
ing. The adhesions thus formed are at first delicate and quite 
cellular, but are later converted into dense, sclerotic bands. 
When fibrinous pleurisy occurs repeatedly, as in tuberculosis 
of the lungs, and is not sufficiently extensive to cause adhe- 
sions, the surface of the pleura may become thickened and 
opaque in spots from proliferation of the connective tissue. 
In this way considerable chronic thickening of the pleura may 
ensue. 

Serofibrinous pleuritis may be simply a further stage of the 
foregoing form, though in many instances it begins almost at once 
as a serous exudation into the pleural sac. The liquid is heavier 
than dropsical fluid and contains flakes and shreds of fibrin. 
Microscopically it is found to contain white and red blood-corpus- 
cles in small numbers, and occasionally detached endothelial cells. 
Sometimes the number of red corpuscles increases considerably, 
and there may be a gradual transition to the hemorrhagic form of 
pleuritis. The amount of liquid varies from a few cubic centi- 
meters to several liters ; and the pleura itself shows a more or 
less extensive coating of fibrinous exudate. The lung is pressed 
backward, as in pneumothorax or hydrothorax, and the adjacent 
organs are similarly displaced. 

Purulent pleuritis, or empyema, or pyothorax, is always the 
result of micro-organismal infection. The process may begin as a 
purulent pleuritis, or as a primary serofibrinous pleurisy, second- 



480 



TEXT-BOOK OF PATHOLOGY. 



ary infection occurring either from within the body or through 
infected aspirating-instruments from without the body. When a 
transition of the latter kind occurs the exudate is seen to become 
more and more turbid ; the number of pus-corpuscles gradually in- 
creases until the liquid is quite purulent. Spontaneous discharge of 
empyema most frequently takes place through the lung and bronchi. 
More rarely rupture occurs through the chest-walls anteriorly be- 
tween the ribs. When rupture has occurred through the lung 
and bronchi the fistulous communication may remain open and 
pneumothorax may ensue: 

The pleura in empyema shows more or less abundant granula- 
tions, which in case of discharge of the liquid serve eventually to 
unite the costal and pulmonary pleura by firm fibrous adhesions. 
Occasionally the pus may be completely absorbed, or it may 
undergo gradual inspissation, remaining as a more or less cheesy 
detritus, which may finally become calcareous. Such terminations, 
however, are rare. 

Hemorrhagic pleuritis is generally the result of tuberculous 
infection or of malignant disease of the lungs and pleura. Pleu- 
ritis may also take a hemorrhagic form in old and cachectic indi- 
viduals, or in persons suffering from scurvy, purpura, and similar 
diseases. As a rule, the liquid is serous, with considerable admixt- 
ure of blood, but in tuberculous and malignant pleuritis it is 
sometimes well nigh pure blood. 

Chronic Pleural Thickening-. — This term is used to include 
cases of thickening of the pleural membrane following various 
forms of pleurisy, and also cases of a progressive productive char- 
acter. To the latter the term chronic pleurisy is, strictly speaking, 
more properly applicable. In either case the pleura is thickened 
by fibrous overgrowth, sometimes uniformly, at other times in 
the form of localized thickenings or adhesions. The subpleural 
pulmonary tissue may become implicated. Eventually the thick- 
ened pleura contracts, and if adherent to the chest-wall may 
cause retractions. The pulmonary tissue is compressed, but the 
bronchi not rarely become atelectatic. 

Associated Lesions in Other Parts. — Though pleuritis is fre- 
quently the result of acute or chronic affections of the lung, it 
often occasions secondary disorders in the latter organ. The sub- 
pleural lymphatics are commonly distended with cells, and the 
inflammatory process may extend for considerable distances along 
these channels into the interlobular septa of the lung. In empy- 
ema the resulting purulent lymphangitis and perilymphangitis 
lead to striking pathologic appearances (see Pneumonia). The 
lung also suffers from direct pressure in serous and purulent pleu- 
ritis. If the compression to which it is subjected is not relieved 
by absorption of the liquid, or by its removal by aspiration, the 
alveolar epithelium degenerates and proliferative inflammation 



DISEASES OF THE RESPIRATORY SYSTEM. 



481 



takes place in the connective tissue, so that a permanent contrac- 
tion of the lung results. The removal of the liquid at this stage 
is not followed by the return of the lung to its proper size and 
function. On the contrary, the removal or absorption of the liquid 
in these cases, especially when they occur in young children, causes 
a sinking in of the ribs and curvature of the spinal column, and 
the heart and other adjacent organs may be permanently dis- 
placed. Most remarkable deformities of the chest may occur. 
Less extensive contraction of one side of the chest, or displace- 
ment of the heart, may result from the contraction of bands of 
adhesions, without marked collapse of the lung. 

Pathologic Physiology. — Acute pleurisy occasions marked local 
symptoms, beginning with sharp pain on the side affected. This 
is usually due to the local inflammation and rubbing of the 
affected parts. There may, however, be extensive neuralgic pains 
radiating from the center of infection. With the development of 
effusion, the pain, as a rule, subsides, as does also the irritative 
cough which attends the first stage, but shortness of breath de- 
velops in correspondence with the amount of effusion. Very ex- 
tensive effusion in the chest may, however, cause even more 
marked pain and tenderness than dry pleural inflammation. The 
infection in simple pleurisy seems to be a mild one, as fever and 
constitutional symptoms are rarely marked. Sometimes the tem- 
perature is a fluctuating one, and sweating and constitutional de- 
pression further suggest suppuration, though the effusion is purely 
serous. Irregular fever and constitutional symptoms of the kind 
indicated are habitual in empyema. 

INFECTIOUS DISEASES. 

Tuberculosis of the pleura, or tuberculous pleuritis, may be 
either primary or secondary. Cases of the former are compara- 
tively rare. In most instances the pleural disease is secondary to 
tuberculosis of the lungs, or to tuberculosis of other adjoining 
parts. Hematogenic infection may occur under the same con- 
ditions as hematogenic infection of the lungs, and frequently the 
lungs and pleurae are studded with miliary tubercles at the same 
time. 

When the pleural disease is secondary to tuberculosis of the 
lungs the appearances vary considerably. In many cases small 
gray or yellow tubercles are found in the subpleural connective 
tissue and in the pleura, and the surface may be coated with 
fibrinous exudate, while the cavity of the pleura may be more or 
less distended with serofibrinous, hemorrhagic, or purulent liquid. 
Not rarely the liquid effusions are reabsorbed and dense adhesions 
are formed, or great thickening of the pleura results. Sometimes 
considerable calcification of the thickened pleura and of the in- 

31 



482 



TEXT-BOOK OF PATHOLOGY. 



spissated exudate is the terminal result. The tubercle-bacilli are 
often difficult to demonstrate in the liquid, even by injections into 
animals, though they may be present in the pleura itself. 

Syphilis of the pleura is a doubtful condition. Fresh pleuritis 
may be found in the neighborhood of a syphilitic gumma ; and 
there are cases of considerable pleural thickening in syphilitic 
persons in which the disease may possibly be syphilitic, though 
in these cases, as in similar indurative conditions in the lungs, 
there is considerable doubt as to the essential nature of the disease. 

TUMORS AND PARASITES. 

Tumors of the pleura are comparatively rare. Fibromata 
and Upomata are occasionally seen as small nodular masses in the 




Fig. 218. — Endothelioma of pleura: the pleural cavity was distended with effusion, and 
the lung was compressed and invaded by secondary nodules. 

serous or subserous coat of the costal or visceral pleura. Chon- 
dromata and even osteomata have been observed. More frequently 
calcification and ossification of portions of the thickened pleura 
take place after pleuritis. 

Primary sarcoma may spring from the subpleural connective 
tissue, and, according to Coats, is especially common in children, 



DISEASES OF THE CIRCULATORY SYSTEM. 483 



and is most frequently of the spindle-cell variety. Primary endo- 
thelioma of the pleura has been studied by a number of investiga- 
tors. In a case under my observation it presented itself as a 
more or less uniform thickening of the pleura of one side, involv- 
ing the diaphragmatic reflection in particular. The cavity was 
filled with hemorrhagic fluid, and there were some nodular enlarge- 
ments on the surface (Figs. 218 and 219). This is the usual ap- 
pearance presented. Metastasis may occur in the lung beneath 
the diseased pleura, or even in more distant parts. 




Fig. 219.— Microscopic section irom the preceding iiinstration. 

Secondary tumors of the pleura may occur by metastasis or by 
direct extension. In the former manner sarcomata and carcino- 
mata sometimes involve this structure ; by the latter method of 
involvement mammary tumors and new growths of the medias- 
tinum, the ribs, or other adjacent structures may extend to the 
pleura. 

Parasites. — Echinococcus cysts may originate in the sub- 
serous connective tissue of the costal or the visceral pleura, and 
may rupture into the pleural cavity. Psorospermise have been 
found in pleural effusions. The Amoeba coli has been found in 
the pus of empyema following hepatic abscess. 



484 



TEXT-BOOK OF PATHOLOGY. 



CHAPTER V. 
DISEASES OF THE GASTROINTESTINAL TRACT. 

THE MOUTH. 

CONGENITAL ABNORMALITIES. 

The most frequent defects in the development of the mouth 
are cleft palate and harelip. In the former of these the entire 
hard palate may be divided, generally to one side of the middle 
line ; and there may be associated harelip and fissure of the soft 
palate. Anteriorly the division occurs between the superior 
maxillary bone and the intermaxillary bone, the fissure of the lip 
being also to one side and often extending into the nostril. The 
soft palate is divided along the middle line, and the uvula may be 
separated into lateral halves. The lip may be cleft on both sides, 
so that there is a small central portion connected with the septum 
of the nose and separated from the lateral portions of the lip. 
Harelip is more frequently unassociated with cleft palate. 

Complete absence of the lips ; or unusual shortness, especially 
of the upper lip ; excessive largeness of the mouth by extension 
of the fissure outward toward the ear ; and imperfect development 
of the lower jaw-bone, are rare congenital conditions. 

CIRCULATORY DISTURBANCES. 

Anemia of the mucous membranes of the mouth is seen in 
cases of general anemia, and is often one of the most striking evi- 
dences of that condition. It is particularly noticeable in the lips. 

Hyperemia. — Active hyperemia occurs in the early period of 
various inflammations, while passive congestion is met Avith as the 
result of obstruction of the circulation in pulmonary and cardiac 
diseases. 

Hemorrhages in the form of small petechia? occur in pur- 
pura and other hemorrhagic diseases, and sometimes in infectious 
fevers. 

INFLAMMATION. 

Inflammation of the mucous membrane of the mouth is termed 
stomatitis ; inflammation of the tongue is designated by the name 
glossitis. 

Stomatitis may be of varying character and intensity. 

Catarrhal stomatitis may result from direct irritation by hot 
liquids or chemical substances, or may occur in depressed condi- 
tions of the general system, possibly as a consequence of infection. 
It is more common in children than in adults. The mucous 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 



485 



membrane of the mouth is red and usually covered with con- 
siderable liquid exudation. When the inflammation is intense 
small vesicular cysts may form from distention of the mucous 
glands, and even localized erosions may appear. When the 
inflammation has continued for a long time, or has been repeated, 
there may form upon the surface silvery-white, slightly elevated 
spots, which result from a hyperplasia of the epithelium, a form 
of keratosis. This condition has been designated by the name 
of leukoplakia. 

Mild catarrhal conditions of the mucous membrane of the 
mouth are especially common on the tongue, the epithelium of 
which constantly desquamates. In the course of gastro-intestinal 
and other diseases the desquamation may be more active, the 
cells, however, being retained upon the surface. Portions of 
food and bacteria cling to the masses of desquamated cells, and in 
this manner the whitish or brownish furring of the tongue so 
commonly met with in various diseases is formed. Sometimes 
the heaping of epithelial cells takes place in localized areas, and 
extends in peculiarly irregular patches, which, from their resem- 
blance to maps, have given rise to the term " geographical tongue." 
In chronic cases the whitish spots of leukoplakia alluded to above 
are formed. Psoriasis of the tongue presents lesions analogous 
to those of the skin. 

Aphthous stomatitis occurs in children under conditions of 
malhygiene and debility, or as a result of gastro-intestinal and 
other diseases. Local irritation often plays an important part. 
There appear in the mucous membrane, especially of the lower 
lip and gums, small whitish spots lying upon an inflamed base. 
Usually these are separated, but sometimes confluence occurs, 
though there is rarely extensive spreading. The whitish mem- 
brane covering or constituting the spots is composed of degener- 
ated epithelium ; and sometimes of fibrin, so that the term croup- 
ous stomatitis may in some cases be applied. The lesions are 
superficial and rarely lead to actual ulceration. It has been held 
that the preliminary lesion is a vesicle ; this, however, does not 
appear to be frequent, and is certainly not essential. 

Foot-and-mouth Disease. — A similar affection occurs in ani- 
mals, particularly in cows, sheep, and goats, and is designated 
foot-and-mouth disease. This condition is contagious, and con- 
siderable epidemics have occurred among persons drinking the 
milk of infected animals. The specific cause is unknown, though 
several micro-organisms have been described. 

Bednar's aphthae are small ulcers found in the mouths of suck- 
ing infants and situated at the lateral portions of the palate over 
the ends of the pterygoid processes, on other parts of the hard 
palate, or occasionally on the soft palate. They are probably 
caused by traumatism occurring in the act of sucking. 



486 



TEXT-BOOK OF PATHOLOGY. 



Ulcerative stomatitis may be met with in various parts of 
the mouth, especially in the gums. In young children it is fre- 
quently the result of malnutrition and lack of cleanliness of the 
mouth. In various cachectic diseases, particularly in scurvy, the 
gums become soft and spongy and tend to ulcerate. Mercuric 
and other forms of poisoning may lead to extensive ulcerations. 
Deeper ulcerations are found upon the sides of the tongue or the 
inner part of the lip in cases of injury due to the sharp edges of 
broken or carious teeth. Ulcerative stomatitis may be secondary 
to necrotic conditions of the bones or suppurative inflammations 
about the roots of teeth. Ulceration beneath the tongue is met 
with in many cases of whooping-cough, and is due to the irritation 
of the teeth in the paroxysms of coughing. 

In ordinary cases of ulcerative stomatitis the gums at the junc- 
tion with the teeth become reddened and soft, and may present 
hemorrhagic infiltration. Later the epithelium of the surface is 
destroyed and open ulcers result. Considerable suppuration may 
occur, and the teeth may be loosened and dislodged. 

A form of disease about the necks of the teeth and secondarily 
involving the gums has been termed pyorrhoea alveolaris. This 
condition seems to result from some constitutional disease closely 
allied to gout. The ligament of the tooth is first inflamed ; sec- 
ondarily retraction and suppurative inflammation of the gums 
occur. The discharge of pus from the gums surrounding the teeth 
gives the disease its name. 

Pseudomembranous stomatitis is most frequently due to the 
action of the bacillus of diphtheria, and is therefore, strictly 
speaking, diphtheria of the mouth. It is usually secondary to 
pharyngeal diphtheria, but may occur primarily upon the lips or 
other parts of the mouth. In some cases of aphthous stomatitis 
the lesion is in reality a pseudomembranous one. 

Phlegmonous stomatitis is more common in the lips than 
in other parts of the mouth, and may be the result of trau- 
matic injuries with intense infection, or a secondary condition after 
facial erysipelas or other cellular inflammations of the face. The 
lips and cheeks may be greatly swollen, and suppuration may 
occur, forming abscesses which tend to rupture into the mouth. A 
chronic form of inflammation of the deeper tissues of the lips may 
lead to hypertrophy. This is especially common in the upper lip 
as the result of long-standing coryza or eczema. 

Gangrenous stomatitis, or noma, affects the mucous membrane 
of the cheeks, and occurs in ill-nourished children, especially after 
measles and other infectious fevers. There is formed a sloughing 
ulcer on the inner side of the cheek, and inflammatory induration 
involving the entire thickness of the cheek. The skin at first 
presents a dark-red or bluish discoloration, and later extensive 
destruction (gangrene) may occur (Fig. 220). The pathologic 



DISEASES OF THE GASTR O-INTESTLNAL TRACT. 487 



changes are those of a rapid necrosis of all the tissues, and micro- 
organisms of suppuration or other saprophytes are usually present. 
Pseudodiphtheria bacilli have been found in a considerable num- 
ber of cases. Putrefactive changes cause a fetid odor. Intense 
septic infection and intoxication generally attend. 




Fig. 220.— Case of noma (Children's Hospital). 



Associated Conditions in Stomatitis. — In many cases the 
inflammation may extend from the mucous membrane of the mouth 
posteriorly to the pharynx. Very commonly the lymphatic glands 
of the neighborhood are involved, and enlargement of the sub- 
maxillary or even the cervical glands is commonly observed. In 
some cases, especially in mercurial stomatitis, the salivary glands 
are coincidently or consecutively swollen and inflamed. Increased 
flow of saliva (ptyalism or sialorrhea) is a frequent symptom. In 
intense cases, especially in gangrenous stomatitis, parenchymatous 
degenerations of other organs may result from general toxemia. 

Glossitis. — Superficial catarrhal inflammations have been 
referred to. More extensive inflammations of the tongue, leading 
to parenchymatous glossitis, may result from injuries, especially 
when accompanied by infection. The entire organ may in these 
cases be swollen, and there is round-cell infiltration with a ten- 
dency to suppuration. Localized parenchymatous glossitis with 
ulceration may occur from injury by carious teeth. 



488 



TEXT-BOOK OF PATHOLOGY. 



Hemilateral glossitis, sometimes attended with the formation of 
herpetic vesicles, is occasionally observed, and is probably depend- 
ent upon disease of the chorda tympani nerve. 

ATROPHY AND DEGENERATIONS. 

Atrophy of the muscles of the tongue and cheeks may occur 
in association with nervous diseases (bulbar palsy). Physiologic 
atrophy of the gums follows loss of the teeth in old age. 

Degenerations of the mucous membrane usually accompany 
inflammations. 

Under the name of nigrities, or black-tongue, is described a 
form of hypertrophy of the papillae of the tongue with pigmen- 
tation. The dorsum of the tongue may be covered with a hair- 
like coating of dark-brown or blackish color. The cause of this 
affection is obscure. 



INFECTIOUS DISEASES. 



Thrush, or parasitic stomatitis, is met with in young 
children, and is due to the action of a micro-organism now 
generally known as O'idium albicans. There are formed upon 
the mucous membrane white patches resembling curdled milk, 
and varying in size from mere points to large areas. These 




Fig. 221 



tend to coalesce and to spread. The mucous membrane is reddish 
and inflamed. The back and sides of the tongue and the inner 
parts of the cheeks are favorite seats. Microscopically the white 
coating is composed largely of mycelial threads of the parasite, 
with which are mingled degenerated epithelial cells and generally 
also other micro-organisms, notably micrococci. The process may 
extend to the pharynx, and sometimes as far as the bronchi or the 
stomach, through the larynx and esophagus. 

Tuberculosis of the mouth may be primary or secondary. 



DISEASES OF THE GA S TR O-INTES TINAL TRACT. 489 



The latter is especially frequent on the root of the tongue, and is 
secondary to tuberculosis of the larynx or pharynx (Fig. 221). 
Small nodular masses of tubercle are formed, and tend to undergo 
cheesy desquamation, forming ulcerated areas. Primary tubercu- 
losis leading to ulceration may occur upon the lips or upon the 
tongue as a result of direct inoculation, as in the kissing of a 
tuberculous person. Nodular masses are formed, which at first 
present themselves as papillary elevations, but subsequently 
undergo characteristic necrosis. The injury of the tongue by the 
teeth, and the favorable soil offered for the retention and multipli- 
cation of the micro-organisms in carious teeth, may play a part in 
the causation. 

Syphilis is most frequently secondary, occurring in the form 
of mucous patches upon the lips or tongue. Gummatous infiltra- 
tion may appear in a localized form, or as an irregular involvement. 
Fissuration and deformity of the tongue may result. The primary 




Fig. 222.— Actinomycosis of the cheek (Illich). 



syphilitic lesion (chancre) resulting from direct inoculation is rarely 
observed. 

Actinomycosis affects the tongue, gums, and jaw-bone, and 
is characterized by a slowly infiltrating process with a tendency to 
necrosis and suppuration, in which the alveolar processes of the 
jaw-bone are generally attacked. The lesion in the mouth may be 
insignificant, while the secondary involvement of the cheeks, or of 



490 



TEXT-BOOK OF PATHOLOGY. 



the lymphatic glands below the jaw and in the neck may be exten- 
sive (Fig. 222). 

TUMORS. 

Cystic formations, due to agglutination of the mouths of the 
mucous glands, are met with upon the tongue and lips. Papillom- 
atous growths of the mucous membrane are also occasionally 
observed. Fibroma, lipoma, myxoma, and even chondroma are 
rare forms of tumors of the submucous tissue of the tongue or 
other parts of the mouth. Not rarely they are congenital. 
Lymphadenoma or lymphosarcoma may occur at the root of the 
tongue, where it takes origin from the lymphatic follicles or the 
lingual tonsil. Sarcoma of other parts of the mouth is rare, ex- 
cepting as an extension from sarcoma of the jaw-bone and other 
parts. 

Carcinoma is the most important new growth of the mouth, 
and in nearly all cases is of the squamous-celled variety. The 
favorite seats are the lower lip, usually toward one side of the 
mouth, and the tongue. It appears as an irregular nodular eleva- 
tion which tends to ulcerate upon the surface and spreads to adja- 
cent structures. Metastasis usually occurs to the submaxillary 
and cervical lymphatic glands. 

Nodular masses having the structure of the normal thyroid 
gland may be found at the base of the tongue. 

Cysts are especially frequent beneath the tongue, at the sides 
of the frenum. These have been termed ranida, and are formed 
by the dilatation of the ducts of the small mucous glands. At 
times ranula may be a cystic dilatation of a duct of the sublingual 
salivary gland or that of a submaxillary gland. Ranula is usu- 
ally found as a rounded or elliptical tumor which may fill the 
floor of the mouth and displace the tongue backward and up- 
ward. The contents consist of somewhat gelatinous albuminous 
liquid. 

Hemangioma, both of the telangiectatic and cavernous varie- 
ties, is occasionally seen, but a more important tumor is lymph- 
angioma affecting the tongue and lips, and giving rise to the 
conditions known as macroglossia and macrocheleia. In these 
conditions there is a uniform enlargement of the tongue or lips, 
and on section distended lymphatic spaces more or less filled 
with liquid and round cells are detected. Such enlargements 
are usually congenital, and are especially met with in cretins. 

THE TEETH. 

Anomalous Development. — Unnatural largeness, or, on 
the contrary, lack of development, is frequently observed. Com- 



DISEASES OF THE ASTRO-INTESTINAL TRACT 491 



plete absence of the teeth has been noted. Numerical increase or 
decrease is frequent. Delay in the eruption of the teeth and 
irregularity in their formation occur in rachitis ; and a form of 
maldevelopment of the upper central incisor teeth of the perma- 
nent set is observed in cases of congenital syphilis (Hutchinson's 
teeth). The characteristics of this condition are the wedge-shape 
of the teeth, the cutting-edge being smaller than the crown, and 
the concave notching of the cutting-edge (see Fig. 106). Hutch- 
inson's teeth are not entirely peculiar to congenital syphilis. 

Caries of the teeth results from malnutrition, digestive 
disturbances, and lack of cleanliness. Micro-organisms which 
lead to acid fermentation contribute in the causation by forming 
acids which soften the enamel and occasion fissures through which 
other bacteria (bacilli and micrococci) may gain entrance into the 
channels of the dentin. The Leptothrix buccalis is commonly 
found in the deposit upon the teeth, but is probably non-specific. 

The carious process consists in a gradual disintegration of the 
enamel and dentin, with the formation of more or less granular 
detritus in which bacteria are abundant. The process may pene- 
trate to the pulp of the teeth and set up a secondary inflammation, 
or pulpitis. Occasionally caries of the teeth begins within. 

Inflammation of the pulp of the teeth may occur in 
association with caries, or sometimes independently. The pulp 
becomes reddened and swollen, and may present hemorrhages and, 
later, suppuration. The inflammatory process tends to spread 
through the roots of the teeth to the tissues surrounding the roots 
and to the alveolar periosteum. Abscesses may thus be formed 
about the teeth, and may spread to the tissue of the gums (alveolar 
abscesses), eventually rupturing upon the surface. 

Tumors composed of tissue resembling the normal dentin are 
spoken of as odontomata. They arise from the pulp during the 
process of development and form irregular outgrowths of the 
crown or roots. Similar outgrowths, resembling the enamel or 
dentin, or cement-substance, are more frequent in later life, and 
have been designated as odontinoids. 

Sarcomata and fibromata may spring from the pulp during the 
development of teeth or from the connective tissue about the 
roots ; and polypoid outgrowths (hypertrophied granulations) from 
the pulp may be met with in association with caries of the teeth 
and pulpitis. 

The most important tumor is the giant-celled sarcoma of the 
alveolar process of the jaw. This is known by the name of 
epulis, though strictly speaking the term is applied rather to the 
situation than to the kind of tumor. Extensive enlargements of 
the jaw-bone and destruction of the surrounding tissues may ensue. 

Cysts are met with in the alveolar processes, and arise from the 
primary follicles in which the teeth are developed. 



492 



TEXT-BOOK OF PATHOLOGY. 



THE PHARYNX AND TONSILS. 

CIRCULATORY DISTURBANCES. 

Anemia of the soft palate and other portions of the pharynx 
occurs in general anemia and in cases of phthisis or other wasting 
diseases. The mucous membrane may be decidedly pallid. 

Active hyperemia or congestion occurs in the beginning 
stages of inflammation and when irritants have been in direct 
contact with the mucous membranes. 

Passive hyperemia is seen in heart-disease, emphysema, 
phthisis, and other chronic pulmonary affections. In these cases 
the mucous membrane is dark red, and not rarely becomes some- 
what edematous. 

Edema of the pharyngeal tissues is found in association with 
inflammatory affections, and may occasion considerable stenosis. 

Hemorrhages may be the result of direct injury, as in the 
swallowing of fish-bones and the like, or may occur in the form 
of petechia? in purpura and other hemorrhagic diseases and in 
intense infections (small-pox, septicemia). 

INFLAMMATIONS. 

Catarrhal pharyngitis, or angina, may affect the entire 
lining membrane of the pharynx, or may be limited to the tonsils 
or other parts. It results from direct irritation by hot liquids or 
chemical substances, from exposure to cold, and particularly from 
infections. Angina, or sore-throat, is met with in many of the 
infectious fevers, or may appear as an independent infection. 

The mucous membrane presents a bright-red color, is some- 
what swollen, and covered with tenacious exudation composed of 
mucus and desquamated cells. Small vesicular elevations may 
form, and after the rupture of these erosions or even superficial 
ulcers are sometimes seen. Occasionally there are hemorrhagic 
extravasations. 

A form of catarrhal pharyngitis, known as herpetic angina, is 
analogous to herpes of the skin, and may accompany facial or 
labial herpes. 

Chronic catarrhal pharyngitis is met with in persons who 
use the voice excessively, especially in the open air. It may also 
result from the abuse of tobacco or alcohol. The posterior wall 
of the pharynx and the pillars of the soft palate are particularly 
involved. The mucous membrane is swollen in the earlier stages, 
but later becomes atrophic, and is marked by slight granular ele- 
vations, which are either hyperplastic lymph-follicles or distended 
mucous glands. The veins in the submucous tissue are enlarged, 
and are visible through the atrophic mucous membrane as tortuous 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 493 



channels. Chronic hyperplasia of the tonsils and chronic laryn- 
gitis are frequently associated. 

Phlegmonous pharyngitis may result from wounds of the 
pharynx, or may be associated with intense infections, such as 
pseudomembranous tonsillitis and pharyngitis, particularly the 
forms due to streptococci. It may result from pustular pharyn- 
gitis in smallpox, or from glanders of the pharynx. Phlegmonous 
tonsillitis sometimes extends to the peritonsillar tissues as far as 
the retropharyngeal wall. 

The soft palate, uvula, arches, or other parts affected are swollen 
and tensely distended. There may be congestion or deep cyanosis 
and edematous exudation. The usual termination is suppuration, 
but sometimes gangrenous necrosis ensues. General septicemia is 
frequently the result. 

Retropharyngeal Abscess. — Phlegmonous pharyngitis primarily 
affecting the retropharyngeal tissues may be due to caries of the 
cervical vertebrae ; occasionally it occurs in the infectious fevers 
in consequence of embolism. 

Pseudomembranous pharyngitis may be caused by the 
Bacillus diphtherias and be truly diphtheritic, or it may be due to 
a variety of other micro-organisms, or to irritating gases, steam, 
and like causes. Non-diphtheritic pseudomembranous pharyngitis 
is especially common as a complication of scarlatina, measles, and 
other infectious diseases, and seems in these cases to be caused by 
the Streptococcus pyogenes. The appearance of the throat may 
be identical with that observed in diphtheria, but extensive 
necrosis is more common, while typical pseudomembranes are less 
frequent. 

The mucous membrane and the underlying parts, especially the 
tonsils, become greatly swollen and edematous ; and subsequently 
suffer necrotic changes. 

There is formed upon the surface of the throat a whitish or 
yellowish patch, or several patches, which tend to coalesce and 
extend from the region of the tonsils to the pillars of the fauces 
and the uvula, or to the mouth, nose, or larynx. The pseudo- 
membrane is quite firmly attached to the mucous membrane, and 
cannot be removed without tearing away part of the underlying 
tissues. Microscopically the deposit is found to consist of gran- 
ular or fibrillar fibrin entangling more or less degenerated leuko- 
cytes and epithelial cells. In the deeper layers intense congestion 
and round-cell infiltration are observed ; in the superficial strata 
degenerated cells and detritus, together with masses of bacteria, 
are conspicuous. 

The neighboring lymphatic glands, notably those below the 
angle of the jaw, enlarge and may suppurate, and sometimes ex- 
tensive cellulitis and suppuration of the floor of the mouth (Lud- 
wig's angina) occur. There are intense systemic intoxication and 



494 



TEXT-BOOK OF PATHOLOGY. 



infection, and secondary lesions are frequently developed in various 
organs (nephritis, myocarditis, etc.). The non-diphtheritic forms 
of pseudomembranous pharyngitis may be distinguished from the 
diphtheritic forms, in typical cases, by the greater intensity of the 
local (necrotic) processes, the earlier and more marked involve- 
ment of the local lymphatic glands, and by the greater tendency 
to nephritis ; but unfortunately atypical cases are very common, 
and an absolute diagnosis can be made by bacteriologic study alone. 

Tonsillitis may be a part of a general pharyngitis, or it may 
occur as an independent affection. Several varieties are described. 

Catarrhal tonsillitis results from the same causes as catarrhal 
pharyngitis in general, and presents similar appearances. The 
tonsils are usually somewhat enlarged. 

Lacunar or follicular tonsillitis occurs from similar causes, and 
may involve the normal tonsil or one affected by chronic hyper- 
trophy. The surface of the tonsil is marked with small white 
or yellowish spots, into which the end of a probe may be 
inserted. These are the lacunae or crypts distended with epithelial 
cells more or less degenerated. Bacteria of various kinds may be 
found in the contents of the lacunae, and doubtless play an im- 
portant part in the etiology. Staphylococci, streptococci, pneumo- 
cocci, tubercle-bacilli, and the bacillus of diphtheria have all been 
observed. The latter two forms may be present merely as acci- 
dental associations, but may possibly play an etiologic part, 




A B 

Fig. 223.— Crypts in cases of tonsillitis : a, acute lacunar; b, chronic hypertrophic ; a, 
surface-epithelium ; b, accumulated contents of crypt ; c, lymphoid follicles surrounding 
crypt (Kaufmann). 

especially the Bacillus diphtheria. Ulceration may occur in the 
walls of the lacunae, and the surface of the tonsil may be consid- 
erably broken down. In other cases the bacteria may penetrate 
the tonsil at the bottom of the lacunae, and phlegmonous tonsillitis, 
or quinsy, may result (see below). The contents of the lacunae may 
be discharged upon the surface, and may adhere for a time as a 
yellowish-white caseous pellicle, resembling diphtheritic pseudo- 
membranes in appearance. In other cases the contents of the 
crypts are retained, undergo inspissation, and may even calcify. 
A certain amount of catarrhal pharyngitis may be associated, but 
the follicular ulcers are rarely seen beyond the tonsils. 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 495 



Phlegmonous tonsillitis, abscess of the tonsil, or quinsy, may be 

the result of simple catarrhal or of follicular tonsillitis, or may be 
associated with phlegmonous inflammation of other parts of the 
pharynx. One or both of the tonsils may be affected. Redness 
and swelling are noted in the earlier stages, but later the mucous 
membrane is pallid or even yellowish. Microscopically diffuse 
round-cell infiltration and eventually focal collections leading 
to abscess-formation are detected. The peritonsillar tissues may 
be involved, and spreading phlegmonous inflammation results. 
Rupture may take place into the pharynx, or the ulceration may 
extend outward, causing discharge upon the neck at the angle of 
the jaw. The internal carotid artery may be perforated. 

Enlargement of the submaxillary and cervical lymphatic glands 
is commonly observed. General septicemia of mild type is not 
infrequent ; myocarditis, endocarditis, and nephritis may result. 
The association of tonsillitis and rheumatism has occasioned much 
discussion. It is very probable that rheumatism frequently results 
from tonsillitis, the latter being the first effect of micro-organ- 
ismal invasion, which eventually causes rheumatism. 

Pathologic Physiology. — Acute tonsillitis may occasion only 
local symptoms, such as pain, difficulty in swallowing, etc., but in 
many cases there are general symptoms — fever, disturbances of 
appetite, etc. The latter vary in severity according to the par- 
ticular infectious cause of the disease. 

Chronic tonsillar hypertrophy may result from repeated attacks 
of simple catarrhal or of follicular tonsillitis. The tonsils are 
enlarged, usually irregularly so, and are harder than normal. On 
section the connective-tissue reticulum and septa are found 
increased, and the lymphoid follicles are likewise hyperplastic. 
Pressure upon the orifices of the lacunae not rarely causes obstruc- 
tion and repeated attacks of lacunar tonsillitis. Retention and 
calcification of the contents of the crypts are particularly common 
in the lacunar tonsillitis of hypertrophic tonsils. Chronic hyper- 
trophy of the tonsils very often occurs in rachitic or badly nour- 
ished children in association with hyperplasia of the lingual tonsil 
and nasopharyngeal adenoid tissues. Distinct evidences of inflam- 
mation are wanting in such cases, and the condition seems rather 
a form of simple hyperplasia of the lymphoid structures. 

PRESSURE=NECROSIS. 

This condition occurs upon the anterior and posterior walls of 
the pharynx, opposite the cricoid cartilage. It is met with in 
marantic persons occupying a dorsal decubitus, and is caused by 
the backward pressure of the cricoid cartilage against the opposite 
vertebra. The mucosa becomes necrotic, and more or less exten- 
sive ulcerations are formed. Complete perforation of the pharyn- 
geal wall sometimes occurs. 



496 



TEXT-BOOK OF PATHOLOGY. 



INFECTIOUS DISEASES. 

Diphtheria of the pharynx usually begins- in the mucous 
membrane covering the tonsils, and spreads to the pillars of the 
fauces, to the uvula, the posterior wall of the pharynx, the cheeks 
and tongue, the posterior nares, or to the larynx. It rarely in- 
vades the esophagus, but may sometimes extend along this struct- 
ure as far as the stomach. 

The specific cause is the Bacillus diphtherise (see Diphtheria, 
Part I.). The characteristic lesion is a pseudomembrane, which is 
formed on the surface and within the mucous membrane. This 
first appears as a grayish or yellowish-white pellicle, more or less 
firmly attached to the mucosa ; it spreads rapidly, and may cover 
the whole of the pharynx in a day or two. In other cases the 
disease progresses slowly, or remains quite limited. The under- 
lying tissues become swollen by inflammatory infiltration (cellular 
and edematous), and swallowing and breathing may then be 
greatly obstructed. When the pseudomembrane is removed from 
the surface a raw and more or less necrotic base is exposed. Mi- 
croscopically the surface of the pseudomembrane is found to con- 
sist of a mass of debris, often containing micrococci and other 
bacteria, as well as the specific organisms, in great numbers. 
Somewhat more deeply the membrane is composed of a fibrinous 
reticulum or masses of fibrin entangling degenerated epithelial 
cells and leukocytes. Still more deeply the tissues of the pharynx 




Fig. 224. — Pseudomembranous inflammation of the uvula : a, masses of micrococci ; 
b, necrotic cells ; c, round-cell infiltration; d, fibrin network (Ziegler). 

are found intensely congested and infiltrated with round cells (Fig. 
224). In the late stages of the disease extensive necrosis of the 
mucosa and submucosa may occur. 



DISEASES OF THE GASTROINTESTINAL TRACT 497 



In some cases diphtheria may undoubtedly present the lesions 
of an ordinary lacunar tonsillitis, and the clinician may be unable 
to determine the nature of the disease. 

Associated Conditions. — Some enlargement of the lymphatic 
glands at the angle of the jaw is usual, and exceptionally this may 
terminate in suppuration. Lesions of the internal organs, espe- 
cially the heart and kidneys, are not infrequent, and disease of the 
peripheral nerves is a common sequel (see Diphtheria, Part I.). 

Pharyngomycosis I<eptothricia. — This condition is met 
with on the tonsils, and less frequently the pillars of the fauces, 
uvula, and other parts of the pharynx. It occurs in persons of 
lowered vitality, and seems to be caused by the Leptothrix buccalis, 
a form of bacterium very commonly met with in the collections 
around the necks of the teeth. The lesions present themselves as 
milky-white and somewhat chalk-like outgrowths arising from the 
tonsillar crypts and the mucous glands. These are often tightly 
adherent, but occasion very little inflammation of the surrounding 
tissues. Microscopically the thread-like parasite is found in 
abundance. 

Tuberculosis may occur in the pharynx in the form of sub- 
epithelial tubercles, which break down and occasion more or less 
extensive ulcerations. 

Tuberculosis of the tonsils may be primary or secondary. In 
the former case infection probably occurs from the invasion of 
the crypts by tubercle-bacilli ; this condition is doubtless more 
common than has generally been supposed. Secondary tonsillar 
tuberculosis usually follows tuberculosis of the lungs or larynx. 
In either case there are formed in the tonsils small tubercles which 
rapidly increase in size, fuse, and subsequently undergo caseous 
change. Discharge of the caseous matter upon the mucous sur- 
face is not unusual, and occasions ulcer-like formations. Second- 
ary infection of the cervical and submaxillar lymphatic glands 
is not infrequent. 

Syphilis may occur in the pharynx in the form of the primary 
lesion or chancre, as mucous patches, or as gummata. The last 
are prone to undergo ulceration with secondary cicatrization. 
Extensive distortion of the pharyngeal structures may be the 
result of the scar-formation. 

Glanders and lepra sometimes invade the pharynx. 

Typhoid ulcers are occasionally met with. 

TUMORS. 

Among the tumors of the pharynx, fibroma, lipoma, chondroma, 
and papillomata are occasionally found on the soft palate, uvula, 
or tonsils. Of the malignant tumors, sarcoma of the tonsils is 
most important. It is usually of the lymphosarcomatous variety, 

32 



498 



TEXT-BOOK OF PATHOLOGY. 



and is rapid in growth and highly destructive. Epithelioma may 
occur at the base of the tongue, in the soft palate, or tonsils. 
Other varieties of cancer are rare. 

Polypoid tumors of the nasopharynx and hyperplastic adenoid 
growths of the same situation frequently extend downward into 
the pharynx proper. 

THE SALIVARY GLANDS. 

Inflammation of the salivary glands affects the parotid most 
frequently. 

Parotitis may be the expression of an independent infection 
(mumps) ; or may be secondary to various infectious diseases, 
such as typhoid fever, typhus fever, or pyemia. 

The specific cause of mumps has not been isolated (see Part L). 
The infection probably occurs through the parotid duct, and in 
some instances inflammations of the mucous membrane of this 
duct have been found to precede the parotitis. The gland is 
swollen and tensely distends its capsule. The inflammatory exu- 
date is probably largely serous, as it may be absorbed and removed 
in the course of a very short time. The disease scarcely ever 
terminates in suppuration. Orchitis is an occasional complication. 

The secondary parotitis occurring in the course of various infec- 
tious diseases is characterized by a marked tendency to abscess- 
formation, and at all stages of the affection round-cell infiltration 
is conspicuous. After the formation of an abscess perforation may 
take place upon the cheek or into the mouth, and sometimes sali- 
vary fistula (see below) are established. Chronic induration of 
the gland may remain after attacks of inflammation. 

The submaxillary gland is occasionally affected with the 
parotid, or independently, in mumps. The sublingual gland 
rarely becomes inflamed. 

Angina I^udovici, or I^udwig's angina, is a septic inflam- 
mation of the tissues of the floor of the mouth surrounding the 
submaxillary gland. It may result from carious processes at the 
roots of the teeth, or from infection of the submaxillary lymphatic 
glands in the course of various infectious diseases, particularly 
scarlet fever. The most frequent termination is abscess-formation, 
with perforation externally or into the mouth. Occasionally rapid 
necrosis or gangrene results. 

Tumors. — The parotid gland is more frequently the seat of 
tumors than the other salivary glands. Benign tumors, such as 
fibroma, lipoma, or chondroma, are rare. The most common new 
growth is the so-called " mixed tumor," which is essentially sar- 
comatous, with the addition of fibroma, chondroma, or myxoma, 
and at times of all these. Epithelioma is rare. 

Diseases of the Salivary Ducts. — Salivary fistula? may 



DISEASES OF THE GASTR O-INTESTINAL TRACT. 499 



result from traumatic injuries or from the perforation of abscesses. 
They most frequently affect the duct of the parotid. 

Concretions composed of phosphate and carbonate of calcium 
are occasionally observed, and may lead to obstruction of the ducts. 

Cystic dilatation of Steno's or Wharton's duct, or of those of 
the sublingual glands, may be due to concretions or to inflam- 
matory processes at the mouths of the ducts. Oval or elliptical 
tumors are formed, and contain transparent, viscid liquid. Such 
cysts belong to the group of conditions designated as ranula, but 
more frequently this is due to obstruction of the small mucous 
glands beneath the tongue. 

THE ESOPHAGUS. 

CONGENITAL DEFECTS. 

Occasionally the esophagus is double, being divided into two 
parts by a septum. Complete absence of the esophagus may occur 
in certain monstrosities ; more frequently there is partial absence 
of the lumen about the middle of the tube. The lower end of the 
esophagus in such cases communicates with the trachea, while the 
upper end terminates as a blind pouch. The intermediate defec-. 
tive portion may be represented by a fibromuscular cord, or may 
be entirely wanting. Fistulous communications may pass from the 
side of the neck to the upper end of the esophagus or pharynx. 
They are due to incomplete closure of the branchial clefts. 

CIRCULATORY DISTURBANCES. 

Anemia may be due to general anemia, and active hyper- 
emia, to the irritation of hot liquids or chemicals. 

Passive congestion results from diseases of the heart or 
lungs, or from cirrhosis of the liver. In the latter condition 
large varicosities may be established in the lower end of the 
esophagus, due to the communications between the left coronary 
vein of the stomach and the esophageal veins. 

INFLAMMATIONS. 

Catarrhal esophagitis is characterized by hyperemia and 
desquamation of epithelium, with very little liquid secretion. It 
may be due to the ingestion of irritating acid or alkaline liquids, 
to scalding, or occasionally to direct traumatic irritation. Super- 
ficial erosions are sometimes met with. 

Chronic catarrhal esophagitis is found in cases of passive 
congestion continued for a long time, and particularly in alcoholics. 
The mucous membrane is thickened and dark in color. Occasion- 
ally erosions are met with, and more commonly areas of hyper- 
trophy of the mucosa. 

Pseudomembranous esophagitis may result from exten- 



500 



TEXT-BOOK OF PATHOLOGY. 



sion of pharyngeal diphtheria or pseudomembranous pharyngitis, 
or it may be primary in rare instances. 

Ulcerative esophagitis may occur as the result of pustular 
eruption in small-pox, or in consequence of irritation of foreign 
bodies. It is not unusual to find small or even large ulcers in 
the mucosa of esophageal diverticula. These are occasioned by 
the retention of food. Peptic ulcers similar to those occurring in 
the stomach are occasionally found in the lower end of the esophagus. 

Phlegmonous esophagitis is rare. It may result from the 
extension of intense inflammation of the mucous membrane into 
the submucous tissue, or to penetration of the mucosa by sharp 
points of fish-bones and the like. 

STENOSIS. 

Stenosis of the esophagus may be due to the pressure of 
tumors or aneurysms upon the esophagus, to the lodgement of 
foreign bodies, to the growth of tumors in the esophageal walls, 
or to stricture of the esophagus. The last most frequently results 
from the healing of ulcerations caused by the swallowing of cor- 
rosive liquids. Syphilitic and post-typhoidal strictures are rare. 
Carcinoma of the esophagus may obstruct by the growth within 
or by the attendant contraction of the walls. 

DILATATION. 

Dilatation of the esophagus may occur in the form of a 
simple dilatation or ectasia, or in the form of diverticula. The 

former variety is common at the lower 
end of the esophagus, and is occasioned 
by obstructions at the cardiac end of 
the stomach, or at the point where the 
esophagus passes through the diaphragm. 
The dilatation may reach considerable 
H size. The mucous membrane is usually 
US thin and often ulcerated. 

Diverticula may be of two kinds, 
those due to pressure from within (pul- 
sion-diverticula) and those due to trac- 
tion from without (traction-diverticula) 
(Fig. 225). The former are more com- 
monly found in the upper portion of the 
esophagus or the lower part of the phar- 
ynx, and arise from the posterior wall 
of the esophagus. They are due to thin- 
fig. 225.— Traction-diverticu- ning of the muscular coat and to her- 

lum of the esophagus (modified • ° . . „ 

from Birch-mrschfeid). mous protrusion or the mucous mem- 

brane. They may reach considerable 
size by gradual distention. The traction-diverticula are most fre- 




DISEASES OE THE G ASTRO-INTESTINAL TRACT. 501 



quently found ne*ar the lower end, opposite the bifurcation of the 
trachea. They are caused by adhesion of diseased bronchial 
glands and subsequent contraction of the attachments. They 
occupy the anterior wall of the esophagus and have a somewhat 
funnel-shape. Perforation may occur, with the development of 
septic infection of the pleura, pericardium, or lungs. Perforation 
of the pulmonary arteries may lead to fatal hemorrhage. 

PERFORATION AND RUPTURE. 

The esophagus may be perforated by necrotic or suppurative 
processes surrounding it, or as the result of ulcers proceeding from 
within. Aneurysms of the thoracic aorta occasionally rupture 
into the esophagus. Retropharyngeal abscesses and phlegmonous 
inflammations of the deep cervical tissues may likewise discharge 
into the esophagus. Perforation by ulcers beginning within may 
be due to the lodgement of foreign bodies, or to the pressure of the 
cricoid cartilage in cases of great asthenia (see Pharynx). Per- 
foration of the lower end of the esophagus may result from pep- 
tic ulcers or esophagomalacia due to regurgitation of gastric liquid 
either before or after death. Spontaneous rupture of the esoph- 
agus occasionally takes place. In these cases there is doubtless 
always some antecedent weakness of the walls. 

INFECTIOUS DISEASES. 

Tuberculosis of the esophagus is extremely rare, and most 
frequently results from extension of tuberculous adenitis of the 
bronchial glands. 

Syphilis occasionally occurs in the form of ulceration and 
cicatrization, leading to stenosis. 

Typhoid ulceration is probably more frequent than has 
been generally thought. Occasionally stenosis is caused by the 
cicatrices of the healed ulcers. 

Thrush may extend from the mucous membrane of the mouth 
and pharynx. 

TUMORS. 

Fibroma, myoma, lipoma, or even sarcoma may occur as some- 
what polypoid submucous tumors, but are rare. Papillomata, in 
the form of outgrowths of the mucous membrane, are more com- 
mon. 

The most important tumor is carcinoma, which is usually found 
in the lower third, generally at the position where the left bronchus 
crosses the esophagus. It may, however, be found at any part. 
The squamous variety is the most common, though a few instances 
of glandular carcinoma are recorded. The tumor usually involves 
the entire lumen of the esophagus, projecting inward and forming 
irregular elevations of the mucous membrane. Later, the growth 



502 



TEXT-BOOK OF PATHOLOGY. 



extends outward through the muscular coat to the fibrous outer 
layer, and even to the surrounding tissues. Dilatation occurs 
above the tumor, and occasionally perforation results from ulcer- 
ations caused by retained food. Local or more distant metastasis 
may take place. 

THE STOMACH. 

CONGENITAL DEFECTS. 

Complete absence of the stomach has been found in certain 
monstrosities ; but stenosis or atresia of the pylorus, division by 
the formation of septa, and hour-glass contractions have been more 
frequently observed. In cases of transposition of the viscera the 
stomach may be reversed in its position, the pylorus being on the 
left side, the cardiac end to the right. 

CIRCULATORY DISTURBANCES. 

Anemia of the mucous membrane is found in cases of general 
anemia, particularly in pernicious anemia. The mucosa has an 
extremely pallid appearance, and is prone to undergo fatty degen- 
eration and atrophy. 

Hyperemia. — Active congestion occurs in the beginning stages 
of inflammation of the mucous membrane of the stomach, and 
results from irritating mechanical or chemical agents. The mu- 
cosa is bright-red in color and may present minute hemorrhages. 
Moderate hyperemia is functional during the period of digestion. 

Passive hyperemia occurs as a result of obstructive heart-dis- 
ease, or more particularly from obstruction of the portal circulation 
by cirrhosis or other diseases of the liver. Pulmonary affections, 
by interfering with the outflow of blood from the right side of the 
heart, may also occasion congestion of the stomach. The mucosa 
is dark-red in color, swollen, and often edematous. Minute 
hemorrhages may occur, and small erosions may appear upon the 
surface. The changes are more marked near the pyloric end of 
the stomach. When the congestion has persisted for some time 
dark-reddish or bluish pigmentation, usually occurring in punctate 
form, is developed and chronic gastritis results. 

Hemorrhage in the mucous membrane or from the mucous 
membrane of the stomach results from a variety of causes. Small 
petechias are met with in active or passive congestion and in acute 
inflammations. They are also present in various infectious or 
hemorrhagic diseases, such as purpura, scurvy, septicemia, and the 
like, and in anemic affections like pernicious anemia. In many 
cases punctiform hemorrhages are developed just before death. 

Larger hemorrhages, and particularly hemorrhages into the 
cavity of the stomach, result from intense passive congestion in 
cardiac disease or cirrhosis of the liver, and from gastric ulcera- 
tion or carcinoma. When large vessels have not been eroded the 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 



503 



blood escapes gradually, and may be vomited in a semidigested 
and disorganized condition (coffee-ground vomit). This is pecu- 
liarly significant of carcinoma. When one of the larger vessels 
has been eroded large quantities of fresh blood may be vomited 
and rapid death may occur. 

llelcena neonatorum, the vomiting of blood by the new-born, 
results from disturbances of circulation due to insufficient respira- 
tion, and possibly in other cases is a variety of infectious hemor- 
rhagic disease. 

INFLAMMATION. 

Acute inflammation of the mucosa, or acute gastritis, 

results from irritation by chemical, mechanical, or thermal agents. 
Some cases are doubtless due to infection. The mucous membrane 
is bright-red and covered with more or less viscid mucous exu- 
date. Punctate hemorrhages may occur. Microscopically there 
are found : marked mucous degeneration of the cylindrical cells of 
the tubules, and desquamation and granular degeneration of the 
cuboidal cells in the fundus of the glands. The mucous mem- 
brane between the tubules is infiltrated with round cells, and not 
rarely the same process occurs in the submucosa. The collections 
of lymphatic tissue (follicles) in the mucous membrane are often 
hyperplastic. Acute gastritis is more frequently found near the 
pyloric end than elsewhere. 

Pseudomembranous gastritis may result from the inges- 
tion of corrosive poisons, and is occasionally seen in small-pox, 
typhus fever, and various forms of septicemia. It may be met 
with in diphtheria, and may be due to direct extension of the 
process along the esophagus. The surface of the mucosa is cov- 
ered with an irregular membrane, and necrosis and ulceration 
are not rarely observed, especially in cases due to corrosive 
poisons. 

Ulcerative Gastritis. — Small erosions may be found in 
cases of extreme congestion or petechial hemorrhage, as well as 
in acute gastritis. Actual ulceration is seen in pseudomembranous 
gastritis, and occasionally as a result of septic embolism in the 
mucosa in cases of malignant endocarditis. Infectious ulcerations 
occur in gastro-intestinal tuberculosis and anthrax, and in typhoid 
fever, but are very rare. 

Chronic gastritis may result from repeated attacks of acute 
gastritis, and is especially prone to occur from improper habits 
of eating, or from the abuse of alcohol. Chronic congestion, such 
as occurs in heart-disease, strongly predisposes. 

Pathologic Anatomy. — The appearance of the mucous mem- 
brane varies greatly. In the milder cases the surface is more or 
less irregular and granular, and is covered with mucous exudate. 
The color may be grayish, but in cases in which passive congestion 



504 



TEXT-BOOK OF PATHOLOGY. 



has preceded the development of gastritis it is often slate-colored 
from pigmentation. 

Microscopically there may be found mucous degeneration of 
the cylindrical epithelium of the tubules, and desquamation and 
not rarely proliferation of the secretory epithelium in the fundus 
of the glands. The glands may be considerably dilated and filled 
with mucous exudate and desquamated cells. The interglandular 
tissues are infiltrated, and may be thickened by the formation of 
new connective tissue ; the same process may involve the sub- 
mucous coat. The blood-vessels of the latter are often greatly 
dilated and their walls may be thickened. In the later stages 
the glands may undergo progressive atrophy, the epithelium dis- 
appearing almost entirely and the lumen of the gland becoming 
less and less distinct. Coincidently with these changes, and 
to some extent causing them, there is fibrous overgrowth of the 
interglandular tissues. 

In some instances the contraction of the new-formed connec- 
tive tissue causes protrusions of the mucous membrane or polypoid 




Fig. 226.— Chronic gastritis, showing polypoid projections of the mucosa. 



elevations (Fig. 226). These may still further enlarge by pro- 
liferation and cystic distention of their glandular elements. In 
other cases the proliferative changes in the interglandular tissues 
may be more diffuse and the mucous membrane more regularly 
thickened. To both of these forms the name hypertrophic gas- 
tritis may be applied. In still other cases the formation of fibrous 
tissue causes pressure-atrophy of the glands ; the surface in these 
cases becomes smooth and the mucosa greatly thinned 

The sclerotic process may involve not only the mucous mem- 
brane, but also the submucous and even the muscular coat. In 



DISEASES OE THE G ASTRO-INTESTINAL TRACT. 505 



such cases the thickness of the wall of the stomach may increase 
greatly, and the size of the organ greatly diminish by contraction. 
The term interstitial gastritis, or gastrophthisis, may be applied to 
such cases. 

Pathologic Physiology in Gastritis. — All forms of gas- 
tritis cause disturbances of the functions of the stomach, desig- 
nated by the terms dyspepsia and indigestion. These disturbances 
are due to abnormal secretion of the gastric glands, reduced motor 
power of the walls of the stomach, and altered conditions of the 
nervous mechanism. The most important alteration of secretion is 
reduction of the amount of hydrochloric acid. This is almost 
constant in uncomplicated gastritis ; in some cases there is practi- 
cally no hydrochloric-acid secretion. The ferments, pepsin and 
curdling ferment, may be produced in insufficient amount, but are 
very rarely absent. In cases in which certain general conditions or 
nervous affections coexist with moderate gastritis, excess of hydro- 
chloric-acid secretion occurs. Reduction in the amount of hydro- 
chloric acid causes delay and inadequacy of digestion of proteids. 
When the acid is wholly wanting decomposition of the proteids 
may occur, and sulphuretted hydrogen and other products of 
decomposition result. Excess of hydrochloric acid interferes with 
salivary digestion in the stomach, and in consequence fermentation 
of carbohydrates, with production of lactic, butyric, or acetic acid 
and of various gases, takes place. Such fermentation, however, is 
not, as a rule, observed unless the motor power of the stomach is defi- 
cient and the food is retained in the stomach beyond the usual time. 
It is not improbable that toxic substances are produced in some cases 
by proteid decomposition, but accurate observations are wanting. 

The motor power is usually deficient in proportion to the inten- 
sity of the gastric disease. In some cases the food is retained 
many hours longer than the usual periods, and fermentation 
and decomposition are thus greatly favored. Dilatation of the 
stomach may be brought about by the retention of food and the 
accumulation of gases of decomposition, and the dilatation in turn 
increases the motor insufficiency of the stomach. 

Altered conditions of the nervous mechanism of the stomach 
manifest themselves in a variety of ways. Sometimes there is 
excessive irritability of the mucosa, causing vomiting ; in other 
cases a feeling of heaviness, or pain. Alterations of appetite and 
of gastric motility are other results probably brought about, in 
part at least, through nervous disturbances. 

The general metabolism suffers profoundly in gastric disease — 
mainly in consequence of the insufficient food eaten or digested. 
Emaciation and systemic depression are the clinical consequences. 
It is probable that toxic substances produced in the stomach 
contribute to the metabolic disturbances, but this remains to be 
proved. 



506 



TEXT-BOOK OF PATHOLOGY. 



PEPTIC ULCER. 

Peptic or round ulcers of the stomach are most frequently 
found in anemic young women, and are probably due to the 
digestive action of the gastric juice. Similar lesions may occur 
in the upper end of the duodenum and in the lower end of the 
esophagus. 

Etiology. — The great majority of the cases occur in young 
women, and particularly in those suffering with chlorosis or 
anemia and general malnutrition. The pathogenesis of these 
ulcers has occasioned much dispute. It is admitted that they are 
due to the action of the gastric juice upon parts of lowered vitality, 
and the term ulcus ex digestione is therefore appropriate. The 
increased acidity of the gastric juice in chlorosis is an important 
factor. The lowered vitality which localizes the ulceration has 
been ascribed to many causes. Embolism or thrombosis with 
infarction was suggested by the shape of the ulcers, and may be 
the explanation for some cases. Spasm of the blood-vessels in 




Fig. 227.— Peptic ulcer, showing erosion into a blood-vessel in the floor of the ulcer 

(Bollinger). 

localized areas, and thickening of the walls of the vessels, leading 
to anemia, have been suggested, as have also direct traumatic 
injuries of the mucous membrane and external traumatism, causing 
rents of the mucous surface. Circulatory disturbances due to 
tight lacing are supposed by some to be important. 

Pathologic Anatomy. — Peptic ulcers may be single, but are 
more often multiple. They are commonly situated in the lesser 
curvature and the posterior wall of the stomach, near the pylorus ; 
occasionally they are found at the fundus or at the cardiac 
end. They vary in diameter from a few millimeters to three or 



DISEASES OF THE GASTRO-INTESTISAL TRACT. 507 



five centimeters. Their shape is characteristic in that they have 
sloping edges, giving them a funnel-form, with the apex toward 
the muscular coat. The edges may be irregular and rough, but 
are often, especially in older ulcers, quite smooth and rounded. 




Fig. 228.— Peptic ulcer with perforation (Bollinger), 



Two dangers are always imminent, hemorrhage and perfora- 
tion. Constant oozing of blood may be due to erosion of the surface, 
and larger hemorrhages may result from ulceration of one of the 
larger arterial branches of the stomach (Fig. 227). Perforation 




Fig. 229.— Stellate scar of a healed ulcer of the stomach (Bollinger). 



is less common than hemorrhage. When the ulcer is situated 
posteriorly perforation is prevented by adhesions attaching the 
stomach to the head of the pancreas or other structures. When 
the ulcer is in the anterior wall perforation is more liable to take 



508 



TEXT-BOOK OF PATHOLOGY. 



place (Fig. 228). The rupture may occur into the peritoneal cav- 
ity or into any of the surrounding structures, and fistulous com- 
munications may be established with the pleural or pericardial 
cavities, or even with the exterior through the abdominal walls. 
Abscesses of the liver, spleen, or pancreas may result from per- 
foration into these organs. 

In the healing of the ulcers scars are formed in the wall of 
the stomach. These have usually a rather characteristic stellate 
shape (Fig. 229). In case of large ulcers extensive scars and 
considerable contraction of portions of the walls of the stomach 
result. Hour-glass contraction of the organ, or pyloric stenosis, 
may follow, and secondary changes, such as gastric dilatation, may 
ensue. Carcinomatous transformation is a not infrequent result 
of long-standing ulceration. 

ATROPHY AND DEGENERATIONS. 

Atrophy of the glands or gastric tubules is frequently seen in 
chronic gastritis. The same condition occurs as a senile change 
and in association with various chronic diseases, especially perni- 
cious anemia. A certain amount of atrophy of the entire mucous 
membrane results in a purely mechanical way from gastric dila- 
tation. 

Decrease in the size of the stomach as a whole may be the re- 
sult of chronic gastritis, when the new-formed connective tissue 
contracts. In such cases the stomach may become quite small, 
the walls, however, increasing in thickness. Somewhat similar 
shrinkage in the size of the stomach occurs in some instances of 
infiltrating cancer of the stomach. The tumor may involve all 
parts of the organ equally, and cause more or less thickening of 
its walls, but the size of the organ is diminished by contraction of 
the connective tissues. 

A form of true atrophy is sometimes caused by obstruction of 
the cardiac orifice ; it is probably due, in part at least, to the in- 
sufficiency of food admitted to the stomach. 

Degenerations of the mucous membrane of the stomach are 
met with in association with inflammation or as independent affec- 
tions. 

Fatty degeneration of the epithelial cells of the glands may be 
the result of intoxications (phosphorus, arsenic), or of conditions 
such as those which lead to simple atrophy. The occurrence of 
atrophy and fatty degeneration of the gastric tubules in cases of 
pernicious anemia is of great importance, though it remains un- 
settled whether these conditions are the cause or result of the 
anemia. Recent investigations would indicate that frequently 
they are the cause. 

Pigmentation is met with as a result of chronic congestion or 



DISEASES OF THE G ASTRO-INTESTINAL TRACT 509 



hemorrhage into the mucous membrane. The mucosa has a dark- 
red or often a slaty discoloration, which is prone to be distributed 
in lines or in circumscribed patches. Bluish pigmentation of the 
stomach sometimes occurs from the ingestion of silver. 

Amyloid degeneration may be found around the blood-vessels 
of the submucosa, or more rarely of the mucosa itself, in cases of 
general amyloid disease. Amyloid ulcerations may occur. 

Calcification has been met with in cases of bone-disease with 
surcharge of the blood with earthy salts. It appears in the form 
of scales or plates of calcification upon the mucosa. 

Gastromalacia, or simple softening of the walls of the stomach, 
is usually a post-mortem condition, and is due to the action of the 
gastric juice. The nature of this process has occasioned much 
discussion, but it is now recognized as a post-mortem condition, or 
as a condition occurring during life only in the agonal period. It 
affects the fundus or posterior part of the stomach. The mucous 
membrane becomes soft and more or less gelatinous, and is grayish 
or yellowish in color if the mucosa was anemic, or brownish in 
cases in which there was congestion before death. Rupture and 
discharge of the contents of the stomach into the peritoneal cavity, 
spleen, or other adjacent organs may occur. The walls of the 
stomach in the affected area show granular degeneration of the 
component cells, but no evidences of inflammatory reaction, and 
when rupture has occurred there are no reactive inflammatory 
lesions of the peritoneum, showing that the perforation occurred 
after death. 

ALTERATIONS IN POSITION AND SIZE. 

Alterations in Position. — The stomach may be displaced 
into the thoracic cavity in cases of perforation or rupture of the 
diaphragm (diaphragmatic hernia). It may be displaced ante- 
riorly as a congenital malposition in consequence of defects of the 
anterior abdominal walls, and may in such cases be quite exposed. 
Downward dislocation, or gastroptosis, is either congenital or ac- 
quired. The acquired form may be due to diseases of the stomach, 
particularly dilatation, to the traction of inflammatory adhesions, 
to enlargement of the spleen, and probably to tight lacing. Occa- 
sionally in anemic and relaxed women all of the abdominal viscera 
tend to descend (splanchnoptosis). 

Dilatation, or gastrectasia, most frequently results from 
obstruction of the pylorus. The latter may be due to cicatri- 
zation the result of the healing of ulcers, to fibroid overgrowth 
and contraction the result of chronic gastritis, or to pyloric carci- 
noma. The pressure of tumors, of a movable kidney, or of aneur- 
ysms may act similarly. At first, pyloric stenosis may be com- 
pensated by hypertrophy of the muscular layer of the stomach, 



510 



TEXT-BOOK OF PATHOLOGY. 



but soon dilatation occurs : food stagnates, fermentation takes 
place, and the dilatation is increased. The mucosa becomes thin 
and ofttimes degenerated and atrophic. 

A second group of cases (atonic dilatation) is independent of 
stenosis of the pylorus, but due to weakness of the walls of the 
stomach. The latter may be the result of chronic gastritis, or 
of a general atonic state. Constant overeating may play an im- 
portant part in some cases. Finally, dilatation may result 
mechanically from abnormal adhesions of the stomach. 

Dilatation of the stomach occasions great stagnation of food, 
and in consequence imperfect digestion and decomposition of the 
food. When hydrochloric acid is absent (as in cancerous stenosis 
of the pylorus and marked atonic dilatation) lactic-acid fermenta- 
tion is pronounced ; when hydrochloric acid is present lactic acid 
is less abundant. Sulphuretted hydrogen and inflammable gases are 
occasionally formed, especially in cases in which hydrochloric acid 
is present. The mucous membrane of dilated stomachs loses its 
absorptive power to a large degree. This, together with the reten- 
tion of ingested liquid in the stomach and the consequent cessation 
of intestinal absorption, leads to great emaciation, and especially 
to desiccation of the tissues. 

Among the micro-organisms met with in the gastric contents 
the Sarcino3 ventriculi are of interest. These occur in bundles of 
peculiar square form. The sarcina is more frequent in non- 
cancerous than in cancerous dilatation. 

INFECTIOUS DISEASES. 

A few cases of tuberculous idceration have been recorded, and 
syphilitic gummata or ulceration may occur. Diffuse cirrhosis and 
ordinary gastritis may be dependent upon syphilis, but the etio- 
logic connection is uncertain. Anthrax may lead to necrotic and 
hemorrhagic ulcers of the mucosa. Thrush is rarely met with, 
though the spores of saccharomyces are frequently present in the 
stomach when the mouth is affected. 

TUMORS. 

Connective-tissue Tumors. — Fibroma, myoma, and lipoma 
are occasionally met with as submucous or subserous polypoidal 
tumors. Sarcoma is rare. It affects the lymphoid tissues of the 
deeper parts of the mucosa, and rapidly spreads to the submucosa 
(Fig. 230). Most cases are of the round-cell variety. Lympho- 
sarcoma of the adenoid tissues of the stomach may be one of the 
lesions of leukemia or Hodgkin ? s disease. 

Epithelial Tumors. — Polypoid elevations, sometimes with 
cystic enlargement of the glands, occur as a result of chronic 
inflammation, and may be large enough to be regarded as tumors 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 511 



in a clinical sense. Adenomatous proliferation of the glands is 
met with in the form of irregular, flat tumors, but these so rap- 
idly become carcinomatous that pure adenoma scarcely exists. 




Fig. 230.— Sarcoma of the stomach, involving all of the coats ; the original growth prob- 
ably occurred in tne mucosa and submucosa. 



Carcinoma is the most frequent tumor of the stomach. It 
occurs in advanced years, and more often in the male sex than in 



Fig. 231— Fragment of carcinomatous tissue found in stomach-washings (Reinevoth). 



the female. The pyloric end of the organ and the lesser curva- 
ture are the favorite sites, but other parts may be affected and the 
entire organ may be involved. Cancer of the stomach may appear 



512 



TEXT-BOOK OF PATHOLOGY. 



as a ring-like swelling of the mucous membrane and submucous 
tissue, surrounding the pylorus and causing stenosis ; as more or 
less circular, flat elevations in the lesser curvature or elsewhere ; 
and, finally, as a diffuse infiltration of the mucosa, submucosa, or 
all of the coats of the entire organ. The mucous surface is 
generally irregularly elevated, and tends to become ulcerated,, 
especially in the soft variety of cancer and in the cases in 
which there are localized flat elevations. Sometimes portions 
of the cancerous tissue may be found in the vomita, and the 
diagnosis of the disease may be thus established (Fig. 231 



Fig. 232.— Carcinoma of the cardiac end of the stomach ; extension into duodenum : Sy 
dilated esophagus ; K, ulcerated carcinoma ; G, a perforating ulceration ; M, stomach 
(Orth). 

Perforation of the wall of the stomach may result from necrotic 
and ulcerative processes (Fig. 232). The neighboring lymphatic 
glands, especially those in the lesser curvature of the stomach, 
are usually implicated through the lymphatic vessels. Direct 
extension to the peritoneum may occur, especially in cases of col- 
loid cancer ; and metastasis through the blood-vessels is extremely 
common. Cancerous emboli are frequently found in the portal 
radicles within the liver, and multiple cancer-nodes of the liver 
are usually found in cases which have existed for some length of 
time. Hematogenous metastasis is most common in soft, ulcer- 
ating cancers. 

Varieties. — There may be distinguished hard or scirrhous 
cancers, soft or medullary cancers, adenocarcinomata or malignant 
adenomata, cylindrical-celled, and squamous-celled carcinomata. 
All forms begin in the mucous membrane and spread rapidly to 
the submucosa. The muscularis may be penetrated and infil- 
tration of the serosa, or even of surrounding tissues, may be 
observed. 




DISEASES OF THE GASTRO-IXTESTIXAL TRACT. 513 

Scirrhous cancer may appear as a circular constricting new 
growth at the pylorus (Fig. 233). In other cases the disease is 
extensive, and the entire organ may be involved by uniform infil- 
tration, and macroscopically the appearance of a simple cirrhosis 




Fig. 233.— Scirrhus of the pylorus, causing pyloric stenosis: D, duodenum ; P, pylorus; 
K, carcinomatous projections on the mucosa (Orth). 

of the stomach is presented. The mucous surface in scirrhus 
rarely ulcerates. 

Encephaloid or soft cancer usually appears as a localized 
tumor at the pylorus or in the lesser curvature. The mucous 




Fig. 234.— Cauliflower carcinoma of pylorus : M, stomach : P, pylorus; D, duodenum 

(Orth). 

membrane is irregularly elevated, ofttimes in a cauliflower man- 
ner (Fig. 234). Ulceration on the surface is common, and hem- 
orrhagic extravasation into the stomach is therefore frequent. 
Metastasis through the blood is liable to occur. Complete per- 
foration of the stomach may take place. 

33 



514 



TEXT-BOOK OF PATHOLOGY. 



Malignant adenoma, or adenocarcinoma, begins as a prolifera- 
tion of gastric tubules. The new-formed acini are, however, 
atypical in arrangement and number, and there is a tendency to 
conversion of the normal cylindrical cells into cuboidal cells, 
and to extensive cancerous infiltration by excessive formation of 
acini or tubules, as well as by destruction of the basement-mem- 
brane of the acini and irregular cellular invasion. The appearance 
of the tumor and its tendencies are the same as those of soft cancer. 

Cylindrical cancer, or cylindrical epithelioma, probably springs 
from the cylindrical lining cells of the stomach, or from the cells 
in the upper parts of the tubules. Atypical tubular aggregations 
of cylindrical cells with a tendency to conversion into cuboidal 
cells are observed. The pylorus is the common seat. 

Squamous cancer occurs at the cardiac end, and generally in 
association with carcinoma of the lower end of the esophagus. It 
is rare. 

Colloid cancer of the stomach appears as a localized, or more 
frequently, diffuse infiltrating, gelatinous new growth of the mucosa 
and submucosa. Rapid extension through the walls of the stom- 
ach and to the peritoneum is frequent. The degeneration may 
affect different forms of cancer, but especially the cylindrical 
variety. The cells and the stroma of the tumor show myxomatous 
degeneration ; and the epithelial elements may in the later stages 
entirely disappear. Extensive invasion of the peritoneum is not 
infrequent. 

Pathologic Physiology and Results. — Carcinoma of the 
stomach is most frequently situated at or near the pylorus, and 
therefore interferes with the propulsion of food. Stagnation of 
the stomach-contents and fermentation result. The latter is 
favored by the absence of hydrochloric-acid secretion so habitually 
observed. In consequence of the stagnation the stomach dilates 
and may reach enormous size, not rarely filling a large part of the 
abdominal cavity. Lactic-acid fermentation is frequently pro- 
nounced. Among the micro-organisms present in the stomach- 
contents a long, thread-like bacillus (Oppler-Boas) has attracted 
much attention, and has been supposed by some to occur only in 
cancer of the stomach. It is certainly frequent, but just as cer- 
tainly not peculiar to the disease. Disturbances of metabolism^ 
with loss of flesh and strength, are marked. 

THE INTESTINES. 

CONGENITAL AND ACQUIRED ABNORMALITIES. 

Occasionally total absence of large parts of the intestinal tract 
is found in monstrosities. Lesser defects, leading to narrowing or 
distortion of the intestines, are more frequent. Marked develop- 
mental defects most frequently occur in the rectum, which may 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 515 



be completely absent, or may be obliterated at the lower end. In 
such cases there may be fistulous communications with the uro- 
genital tract, or there may be a persistent cloaca, as in fetal life. 

Congenital Enlargement of the Intestines. — The colon 
is most apt to be affected, and may be greatly enlarged. 

Diverticula. — Localized dilatations, constituting diverticula, 
are frequent, the most common form being the Meckel's diverticu- 
lum. This usually arises from the ileum, about a meter above the 
ileocecal valve, and is attached to the intestine opposite the mesen- 
tery. It represents the remains of the omphalomesenteric duct 
of fetal life. Occasionally it has been found patulous to the um- 
bilicus. More commonly there is merely a short diverticulum of 
the intestines, varying from a few to several centimeters in length, 
and having a closed extremity which may be somewhat dilated. 
The extremity may be connected with the umbilicus by a cord, 
but is usually free. 

Diverticula are also formed in later life. Very commonly, in 
cases of constipation, small pouchings or dilatations occur in the 
large intestine, particularly in the descending colon and rectum. 
Another form affects the small intestine more commonly than the 
large boAvel. In this there are found small pouches lying near the 
mesenteric attachment, and owing their origin to localized weak- 
ness or separation of the muscle-fibers of the bowel. Protrusion 
of the mucosa takes place, probably, as a result of pressure from 
within ; and the pouch is therefore a hernious projection of the 
mucosa and serosa. Such diverticula may be multiple or single. 

Congenital Abnormalities in Position. — The position of 
the several parts of the intestinal tract may vary widely from the 
normal. Not rarely the ascending colon and cecum are situated 
on the left side ; the sigmoid flexure and descending colon being 
on the right side. Other abnormalities of position, of less practi- 
cal importance, are frequent. 

Knterocystoma. — A congenital cystic condition found at 
the umbilicus has been described as cystic dilatation of parts of 
the original omphalomesenteric system of the fetus, and has been 
named enterocystoma. 

Dilatation. — More or less uniform enlargement of the intes- 
tines may result from long-standing constipation. Enormous 
dilatation of the colon is sometimes seen. In this the wall of the 
intestine undergoes compensatory hypertrophy, and small pouch- 
ings or diverticula are commonly observed, especially in the rectum. 

Narrowing, or stenosis, of the intestine at any part may be 
due to pressure of new growths or displaced viscera, to cicatricial 
constrictions following ulcerations, or to neoplasms. Cicatricial 
stenosis is particularly common in the rectum following dysenteric 
ulcer. Narrowing of the lumen may be due to an ingrowth of car- 
cinoma or the presence of papillomatous or polypoid tumors within. 



516 



TEXT-BOOK OF PATHOLOGY. 



Hernia. — This term is applied to malposition of any of the 
viscera, with displacement of the organ from the cavity in which 
it normally lies ; but it has been more particularly applied to such 
displacements of the intestines ; and the single term hernia is 
significant of intestinal hernia. 

Occasionally hernise are congenital ; more often they are 
acquired. Hernia occurs at the points where the abdominal walls 
or the peritoneum is naturally weak from the emergence of vessels 
or the existence of natural outlets. 

Etiology. — The predisposition to hernia may consist in un- 
natural weakness of the abdominal wall, especially at the points 
where hernia is likely to occur, resulting from imperfect 
closure of such portions or from general muscular weakness. 
Abnormal movability of the intestines, resulting from natural or 
acquired elongation of the mesenteric attachments and increased 
weight of the abdominal contents from the deposit of peritoneal 
fat, contributes largely to the formation of hernise. The imme- 
diate exciting cause in many cases is strain, and probably in all 
cases repeated strain helps in the development of the protrusion. 
The most frequent form of ventral hernia is the umbilical, which 
occurs especially in infants as the result of imperfect closure of 
the abdominal walls at the umbilicus. 

There may be distinguished two groups or yarieties — the inter- 
nal and the external hernia?. 

Internal Hernia. — By this term are designated hernious dis- 
placements of the intestines into other cavities within the body, 
the most important being upward displacement into the thorax 
through congenital or acquired clefts of the diaphragm (diaphrag- 
matic hernia); and backward displacement through the peri- 
toneum into the retroperitoneal space (retroperitoneal hernia). 

External hernia may be inguinal, femoral, ventral, vaginal, 
rectal, perineal, ischiatic, or obturator. The most frequent of these 
are the inguinal and the femoral. In the former the protrusion may 
occur through the external inguinal ring, the intestine descending 
through the inguinal canal, sometimes as far as the scrotum (in- 
direct inguinal hernia). In another group of cases the intestine 
pushes directly forward through the internal inguinal ring, and 
may present anteriorly under the skin, or may descend through 
the lower part of the inguinal canal to the scrotum (d irect inguinal 
hernia). The indirect inguinal hernia? are sometimes congenital, 
and are due to the failure of closure of the peritoneal reflection 
which passes downward through the inguinal canal. 

Femoral hernia? are especially common in women, and are 
formed by the protrusion of the intestine through the femoral 
ring, the hernia presenting on the inner side of the thigh, at the 
position of the saphenous opening. 

Pathologic Anatomy. — The hernia consists of a sac or wall 



DISEASES OF THE G ASTRO-INTESTINAL TRACT 517 



and of the contents of the hernia. The sac is usually constricted 
at its junction with the general peritoneal cavity (neck), and dis- 
tended and dilated outside of or below this point (fundus or body 
of sac). The sac of the hernia is always lined with the protruded 
portion of the peritoneum. The contents of the hernia may be 
coils of intestine or portions of omentum, or both. Most fre- 
quently some part of the small intestine occupies the hernia, and 
sometimes simply a Meckel's diverticulum has been discovered. 
In rare cases the sigmoid flexure or other parts of the great bowel 
may be found. 

Secondary changes often ensue. Inflammation of the lining 
membrane of the sac and of the intestinal coils may lead to fibrous 
adhesions constricting the neck of the sac and binding the intes- 
tines firmly in place. If the contents of the hernia have receded, 
such inflammation may obliterate the sac completely or merely at 
its neck, the body of the sac in the latter case becoming distended 
with serous liquid. In cases in which portions of omentum are 
included in the hernia hypertrophic overgrowth of the adipose tis- 
sue may occur, and may lead to appearances not unlike those of a 
lipoma. 

Hernise are described as being reducible and irreducible, accord- 
ing to the ability of replacing the contents into the peritoneal 
cavity or not. Hernise become irreducible when the coils of 
intestine are distended by the accumulation of fecal matter, when 
fibrous adhesions have narrowed the neck of the sac or bound the 
coils firmly in place, or when additional coils of intestine or por- 
tions of the omentum have descended into the hernia. 

Strangulated Hernia. — This term is applied to hernise in which 
pressure at the neck by inflammatory exudation or constriction, or 
inveterate obstruction by accumulating contents of the bowel, has 
led to obstruction of the circulation in the intestinal coils of the 
hernia. Intense passive congestion, inflammation of the peritoneal 
covering of the intestines within the hernia, and, finally, gangre- 
nous necrosis are the frequent results. 

INTESTINAL OBSTRUCTION. 

Complete obstruction of the intestines, or ileus, may be due to 
internal strangulation by bands of adhesions, to a twist or volvulus, 
or to intussusception or invagination. 

Internal strangulation may be due to the obstruction of a 
coil of intestine by fibrous peritoneal adhesions, or by a coil slip- 
ping through abnormal openings or perforations in the mesentery 
or omentum. The persistence of the cord passing from the end 
of a Meckel's diverticulum to the umbilicus is an unusual cause. 

The results of internal strangulation are generally serious. 
Great dilatation occurs above the point of obstruction, the intes- 



518 



TEXT-BOOK OF PATHOLOGY. 



tine below becoming collapsed. Great congestion and subse- 
quently peritonitis occur at the point of stricture, and necrosis 
with perforation may ensue. 

Volvulus is the term applied to a twist of some part of the 
intestinal canal. Occasionally there is simple rotation of the 
bowel about its own axis, but more commonly a loop of intestine 
twists about its mesenteric attachment. Abnormal laxity of the 
mesentery is an important predisposing cause, and may be a con- 
genital condition, or may result from the absorption of fatty 
deposit between the mesenteric layers. The immediate cause is 
generally strain or abdominal compression. 

The most frequent seat of volvulus is the sigmoid flexure. 
The bowel above the point of obstruction becomes distended, as in 
internal strangulation, while the coil included in the twist itself is 
engorged with blood and frequently presents hemorrhagic infarc- 
tions in consequence of the obstruction of the vessels in the mesen- 
tery. Complete knots are occasionally observed in volvulus. 

Intussusception, or invagination, is a condition in which 
one part of intestine slips into an adjoining part, as one may in- 
vert the finger of a glove (Fig. 235). The 
upper part of the intestine is usually indupli- 
cated and pushed into the lower part. Ir- 
regular peristalsis, resulting from intestinal 
disorders, and particularly from atony of one 
part with increased activity of adjoining 
parts, is the most frequent cause. Occa- 
sionally polypoid tumors within the bowel 
are dragged forward by the peristalsis, and 
carry the higher part of the intestine to 
which they are attached into the lower part. 
Intussusception is more common in children 
than in adults, and affects the ileocecal region 
most commonly. Not infrequently multiple 
invaginations are found in the small intes- 
tine of children ; these probably occur during 
the death-agony or post-mortem. 

The appearance of intussusception is sim- 
ply that of one part of intestine pushed into 
the adjoining part, with secondary inflam- 
matory and congestive changes. Most fre- 
quently invagination begins at the ileocecal 
region, the valve and ileum being carried 
forward into the ascending colon. Very 
rarely the ileum itself invaginates through the valve. The 
attachment of the mesentery leads to a sharp angulation of the 
area of invagination, and the extent to which the protrusion may 
occur will depend upon the length of the mesentery. Occasionally 




Fig. 235.— Intussuscep- 
tion (from a specimen in 
the Museum of the Phila- 
delphia Hospital). 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 519 



the ileocecal valve may be carried through the colon and rectum 
and present externally. The adjoining serous surfaces of the in- 
vagination tend to unite by peritonitis, and the intussuscepted 
portion may become gangrenous and be discharged. If peritonitis 
has established union between the ensheathed and the ensheathing 
section of the gut, recovery may ensue. Otherwise the perforation 
leads to fatal peritonitis. 

PROLAPSE OF THE RECTUM. 

Prolapse of the rectum in consequence of weakness of the 
sphincter and other parts of the wall, together with repeated 
straining, is a common condition in infants, and is occasionally 
met with in adults. In children any form of diarrhea may be 
complicated by prolapse ; in adults chronic proctitis is the most 
frequent cause. The weakened condition of the sphincter in 
proctitis furnishes the predisposition, and the characteristic tenes- 
mus of the disease is the immediate cause. Prolapse may be only 
an occasional condition, or may be constant. Secondary inflam- 
mation, ulceration, and even necrosis of the prolapsed portion 
may occur. 

ATROPHY AND DEGENERATIONS. 

Atrophy of the mucosa is frequently met with as a part of 
chronic enteritis in its later stages. This is especially marked in 
young children suffering from chronic intestinal catarrh and 
marasmus. Occasionally atrophy of the mucosa or of all of the 
coats of the intestines may occur as an independent affection, as 
the result of marantic or cachectic conditions. 

Pigmentation. — Pigmentation may be due to hemorrhages 
in the mucosa or submucosa, and not infrequently after intense 
hemorrhagic inflammation the bowel may be quite black from the 
deposit of hematogenous pigment. Brownish pigment deposited 
in the muscle-cells, analogous to that of brown atrophy of the 
heart, is occasionally observed in old and cachectic individuals. 
Similar pigmentation of the muscle-cells and also of the submucosa 
or mucosa, of even more decided character, occurs in youthful 
persons addicted to alcohol. The intestines alone may be thus 
affected, or the liver, spleen, and lymphatic glands are simulta- 
neously involved. The term hematochromatosis has been pro- 
posed for this condition. 

Amyloid degeneration is met with in association with amy- 
loid disease of the liver, kidneys, or spleen, and particularly in 
cases in which there is tuberculous ulceration of the intestines. 
The mucous membrane is principally involved, and becomes some- 
what hardened and presents a peculiar grayish luster. Superficial 
erosions and even considerable ulcers may result. The process 
begins, as elsewhere, in and around the small blood-vessels. 



520 



TEXT-BOOK OF PATHOLOGY. 



CIRCULATORY DISTURBANCES. 

Active hyperemia may occur from acute irritation, and 
forms a part of inflammation. 

Passive hyperemia results from causes similar to those 
producing congestion of the stomach. Among these, obstructive 
diseases of the liver, notably cirrhosis, and cardiac and pulmonary 
affections are most prominent. The intestinal mucosa becomes 
somewhat swollen, ofttimes edematous, dark bluish-red in color, 
and occasionally marked by punctate hemorrhages. The mesen- 
teric veins are widely dilated. Occasionally hemorrhagic liquid 
is found within the intestines, the points of hemorrhage remaining 
undiscovered. 

Hemorrhage. — Petechia? are found in many cases of violent 
septic or infectious diseases, in intense anemias, and as the result 
of marked passive hyperemia. Embolism in cases of ulcerative 
or malignant endocarditis may lead to petechial hemorrhages, and 
the same are observed as a part of the morbid anatomy of intes- 
tinal anthrax. Large intestinal hemorrhages may occur from 
typhoid, tuberculous, dysenteric, or syphilitic ulcerations, or from 
the perforation of a large arterial branch by a peptic ulcer in the 
duodenum. Hemorrhoids may occasion considerable hemorrhages 
from the rectum. 

I^dema of the mucosa may result from passive congestion, and 
attends acute or chronic inflammations, especially the more intense 
forms. 

Embolism and thrombosis of the mesenteric arteries are 
rare conditions. Embolism may lead to hemorrhagic infarction. 

Hemorrhoids result from varicose enlargement of the veins 
of the rectum. They are usually found in the lower part of the 
rectum, inside or outside the sphincter, and a distinction is made 
between internal and external hemorrhoids. 

Etiology. — Obstruction of the venous circulation is the import- 
ant etiologic factor. It may be due to chronic diseases of the liver 
(cirrhosis), repeated pregnancies, pelvic tumors, or chronic consti- 
pation with frequent retention of feces in the rectum. The last- 
named condition acts in a twofold manner. On the one hand, it 
causes venous obstruction, and, on the other hand, chronic proctitis, 
which in turn occasions disease of the veins of the rectum, and thus 
predisposes them to dilatation. In all cases of hemorrhoids, con- 
stipation and the resulting proctitis are important as auxiliary 
causes. Hemorrhoids are rarely met with before adult age. 

Pathologic Anatomy. — The hemorrhoid presents itself as a small 
polypoid elevation of more or less congested appearance. On 
section it is found to be highly vascular, and to consist of dilated 
veins. There may be a congeries of slightly enlarged veins or 
cavities of considerable size. Between the veins there is more or 



DISEASES OF THE GA STR O-IXTESTJXA L TRACT. 521 



less abundant inflammatory connective tissue. Thrombosis often 
occurs within the cavities ; and occasionally the fibrous tissue 
around them undergoes active proliferation, when a structure 
resembling fibro-angiomata results. Hemorrhagic extravasations 
may occur from the veins, and free hemorrhage from the surface 
is a common symptom. Infective inflammation and phlebitis of 
the veins sometimes occur. In these cases the hemorrhoid en- 
larges and becomes inflamed and edematous. Inflammation of 
the adjoining tissues may occur (proctitis, periproctitis). 

Hemorrhoids may cause marked anemia by the repeated hem- 
orrhages, and sometimes occasion septic infections when they have 
themselves become infected and inflamed. 

INFLAMMATIONS. 

Inflammation of the intestines, or enteritis, may affect 
any part of the intestinal canal, and involve the mucosa and sub- 
mucosa more particularly. It is more frequently present in chil- 
dren and in the aged than at other periods of life. 

Etiology. — The causes of enteritis are similar to those of gas- 
tritis, and among them may be reckoned all forms of irritating 
foods or foreign matter taken with the food. Poisons of various 
kinds operate in a similar manner. In many cases the irritant 
poisons which occasion enteritis are developed within the body in 
consequence of improper digestion and fermentation. Bacteria 
play an important role in this process, and sometimes are them- 
selves the direct cause of enteritis in instances in which impro- 
prieties of diet or digestive disturbances have furnished favorable 
conditions for their growth and multiplication. The normal colon- 
bacillus is perhaps the most frequent and important micro-organ- 
ism of ordinary non-specific enteritis, but other organisms doubt- 
less frequently play a part. The colon-bacillus probably increases 
in virulence under certain conditions and then occasions irritation. 

Pathologic Anatomy. — There are a number of varieties of ente- 
ritis, and different types may be described, though individual cases 
rarely conform to a single variety. Of the acute forms of enteritis, 
the important are the catarrhal, suppurative, and the pseudomem- 
branous. 

Catarrhal enteritis may affect any part of the intestinal tract. 
The mucosa is swollen and usually light-red in color ; the arteries 
are visibly distended, and not rarely there are petechial hemor- 
rhages. The surface is covered with mucous exudate containing 
desquamated and degenerated epithelial cells and emigrated leuko- 
cytes ; while the intestinal contents are rendered liquid by serous 
exudation. The solitary follicles or agminated collections of 
lymphoid tissue may be particularly swollen and cause projections 
above the surrounding mucosa. The term follicular enteritis is 



522 



TEXT-BOOK OF PATHOLOGY. 



applied to such cases. In other instances the desquamation of epi- 
thelium is more prominent than the mucous exudation, and con- 
siderable shreds of mucosa may be loosened and discharged. The 
term croupous enteritis is suggested by such conditions. 

Suppurative enteritis differs from the catarrhal form in the 
greater degree of emigration of leukocytes. The exudate upon 
the surface may be largely composed of white corpuscles, and in 
intense cases the surface may be covered with almost pure pus. 
Round-cell infiltration of the mucosa and the submucosa is 
present, and focal collections leading to submucous abscesses or 
to ulcers upon the mucous surface are occasionally seen. The 
solitary follicles are enlarged and tend to break down, forming 
follicular ulcers. 

Ulceration of the intestines occurs in a variety of conditions. Peptic 
ulcers, similar to those met with in the stomach, are occasionally found in 
the duodenum. They have the same characters and tendencies as those of 
the stomach ; they may occasion sudden death from hemorrhage. Ulcers 
in the duodenum are also an occasional result of extensive burns of the 
skin ; and recently attention has been called to the frequency of duodenal 
ulceration in cases of chronic Bright's disease. Ulcerations of the ileum 
are habitual in typhoid fever and tuberculous enteritis, and are occasion- 
ally due to anthrax or actinomycosis. Ulcers may be found in all forms of 
enteritis of childhood, especially in intense forms and in cases complicating 
the exanthemata. Sarcomata and carcinomata are rare causes. Ulcera- 
tions of the large bowel are met with in chronic enteritis and dysentery. A 
form of peculiar clinical interest is anal fissure. This is a linear ulceration 
of the rectum in the region of the sphincter. It may be associated with 
hemorrhoids or may be independent. 

. Pseudomembranous enteritis is characterized by the forma- 
tion of a grayish membrane upon the surface of the intestine. 
The large intestine is more frequently involved, and the process 
is especially met with in dysentery (see p. 527). True diphtheria 
of the bowel with pseudomembranous deposit may sometimes occur. 

Chronic enteritis results from acute attacks or from repeated 
irritation. Chronic congestion in consequence of hepatic or car- 
diac affections is a predisposing cause of importance. 

In the early stages the mucous membrane is usually more or 
less swollen, and sometimes proliferative changes in the glandular 
elements may lead to distinct polypoid elevations. These are 
especially pronounced in cases in which the healing of ulcers of 
acute enteritis has occasioned cicatricial constrictions and thus 
elevated adjoining parts of the mucosa. The elevated portions 
may undergo proliferative inflammation, and polypoid formations 
result. In the later stages of chronic enteritis atrophy may ensue, 
in part as the result of the overgrowth of the stroma of the mucosa 
and the degeneration of the glandular elements, in part also as the 
result of the overdistention or tympany resulting from fermentation 
of the intestinal contents. This atrophy may affect the mucous 
membrane alone, but more commonly also involves the muscularis. 



DISEASES OF THE 



GASTR O-INTESTINA L 



TRACT. 



523 



Hyperplastic processes in the lymphoid elements may be a promi- 
nent feature in the hypertrophic stage of chronic enteritis, and may 
give place to atrophy in the later stages. On the other hand, the 
enlargement of the solitary follicles and Peyer's patches may per- 
sist for a long time after atrophy has led to great thinning of the 
remaining portions of the mucosa. 

Pathologic Physiology. — Enteritis may occasion profound dis- 
turbances in a variety of ways. In cases of infective character 
general systemic intoxication may result from the absorption of 
bacterial products or substances resulting from decomposition 
of the intestinal contents. In other cases the intensity of the 
local irritation may, through the nervous system, occasion great 
depression or shock ; and subsequently the exudations into the 
intestines may cause depletion of the vascular system and failure 
of the circulation. The local effects and the resulting behavior of 
the bowels differ in different cases. Sometimes the peristaltic 
movements are arrested by the intensity of irritation and obstinate 
constipation results ; more frequently hurried peristalsis and the 
abnormal exudation (serous or mucous) occasion diarrhea. The 
digestive processes fail from the diseased condition of the bowel, 
as well as from the rapid peristalsis and premature discharge of 
the intestinal contents; more or less profound disturbance of 
health results. 

INFLAMMATIONS OF SPECIAL PARTS. 

Duodenitis. — Duodenitis occurs in association with gastritis 
from irritating food and the like. The appearances are the same 
as in gastritis. Duodenitis is prone to occasion obstruction of the 
terminal portion of the common bile-duct by the inflammatory 
thickening of the mucosa and the accumulation of mucus in the 
mouth of the duct ; and in this way gives rise to obstructive 
jaundice (catarrhal jaundice). 

Inflammation of the ileum presents no special charac- 
teristics, excepting that enlargement of the follicles (follicular 
enteritis) is frequently conspicuous. Follicular ileitis is particu- 
larly common in children suffering from infectious fevers, such as 
diphtheria and scarlatina. Peyer's patches may be considerably 
enlarged and even ulcerated. The ulcers are generally small, and 
several may occur in a single Peyer's patch instead of single ulcers, 
such as occur in typhoid or tuberculous enteritis. 

Typhlitis or cecitis (inflammation of the cecum) may be 
due to the irritation of the intestinal contents in consequence of 
constipation (stercoral typhlitis). This affection is probably very 
frequent, though it leads to no severe consequences and occasions 
no urgent symptoms. Typhlitis is probably generally of the 
simple catarrhal variety, but in obstinate constipation or obstruc- 
tion of the colon ulceration may occur. Perforation or extension 



524 



TEXT-BOOK OF PATHOLOGY. 



to the surrounding tissues {perityphlitis) is the rarest of all conse- 
quences. Usually the latter is secondary to inflammations of the 
appendix vermiformis. 

Appendicitis may be a primary condition, or it may result 
from primary typhlitis or cecitis. The inflammation of the 
mucosa of the cecum may extend directly to that of the appendix ; 
or may cause obstruction of the mouth of the appendix in the 
same manner as duodenitis causes obstruction of the common bile- 
duct. There results a retention of the contents of the appendix 
and multiplication with increased virulence of the contained 
bacteria (Bacillus coli communis, staphylococcus, streptococcus, 
and others). The mucosa of the appendix, rendered less resistant 
in consequence of the overdistention and associated congestion, 
may be penetrated by the micro-organisms and appendicitis 
results. In many cases fecal concretions are found within the 
appendix, and less commonly foreign bodies of various sorts have 
been found. These have been assumed to be the direct cause of 
the disease, and doubtless may play a part by irritating the mucosa, 
or injuring it in such manner that micro-organisms easily pene- 
trate it. On the other hand, there is much reason to believe that 
the fecal concretions are often formed in consequence of the 
accumulation of mucous and desquamated epithelial cells and the 
stagnation of the contents of the appendix, after the disease has 
begun. Typhoid and tuberculous ulcers and actinomycosis have 
been found in the appendix. These lesions may occasion sec- 
ondary appendicitis of an ordinary sort, or they may in them- 
selves cause the symptoms of appendicitis. Obstruction of the 
arterial supply of the appendix was formerly regarded as an im- 
portant element in the etiology, but probably is only of secondary 
importance. Appendicitis is less frequent in women than in men. 
This has been ascribed to the existence of a more adequate blood- 
supply (the extra part derived from the ovary) in women. 

Pathologic Anatomy. — The pathologic anatomy of appendi- 
citis varies in different cases, and we may, for convenience, dis- 
tinguish a catarrhal, a necrotic or gangrenous, and an interstitial 
form. 

In the mildest or catarrhal form there is merely retention of 
the contents of the appendix and slight disease (swelling and 
erosion) of the mucosa. The muscularis and serous coat may be 
congested and edematous, but are not extensively involved. The 
contents of the appendix are more or less mucopurulent in char- 
acter. 

In the necrotic or gangrenous form the mucous membrane suf- 
fers rapid destruction and the muscular and serous coats are quickly 
invaded. Fibrinous peritonitis soon develops in the serous coat 
and over the adjacent intestines, either as a result of penetration 
of bacteria through the walls of the appendix, or in consequence 
of perforation of the walls. The local peritonitis serves the pur- 



DISEASES OF THE G ASTRO-INTESTINAL TRACT 525 



pose of restraining the infective disease and prevents diffuse peri- 
tonitis. In cases of rapid gangrene, with early rupture or escape 
of abundant bacteria, general peritonitis may result before a re- 
straining wall can be formed. 

The term interstitial appendicitis may be used to designate 
cases in which all of the coats of the appendix are involved and 
in which there is a special tendency to productive changes in the 
connective tissues. In reality all cases of appendicitis show more 
or less interstitial change of 
this character (Fig. 236) ; but 
in some it is the conspicuous 
feature. These cases fre- 
quently terminate in chronic 
thickening of the appendix. 

Results. — Mild cases of ca- 
tarrhal appendicitis may sub- 
side after free purgation, with 
relief of the obstruction at the 
mouth of the appendix. In 
more serious inflammations 
and in cases in which the 
obstruction remains, the dis- 
ease spreads through the walls 
of the appendix to the perito- 
neum and occasions local peri- 
tonitis ; or rupture of the ap- 
pendix occurs, and more in- 
tense local or general perito- 
nitis follows (Fig. 237). In 
either case fibrinous deposits 
are formed upon the perito- 
neum, and not rarely a local- 
ized abscess (perityphlitic ab- 
scess) results. The appendix 
itself may be separated from 
the cecum, and may lie free in 
the abscess, or it may be firmly 
embedded in the fibrinous wall 
of the abscess. The latter may 
subsequently undergo inspissa- 
tion, but more commonly rup- 
tures into the general perito- 
neal cavity, into some part of 
the intestines, into the ureter, 
bladder, or externally. In 
cases with favorable outcome the appendix is usually bound down 
by adhesions, attaching itself to neighboring coils of intestine or 
to other structures. The appendix in such cases is usually dis- 





Fig. 236.— Acute appendicitis, with round- 
cell infiltration and hyperplasia of connective 
tissue in all of the coats. In large part the 
round cells of the mucosa and submucosa be- 
long to the normal lymphoid tissue of these 
parts. 



526 



TEXT-BOOK OF PATHOLOGY. 



torted and greatly thickened, and repeated attacks of inflammation 
{^relapsing or recurring appendicitis) are not unusual. 

There is generally more or less systemic intoxication and infec- 
tion, and secondary lesions may be found in distant organs. JSTot 
rarely pylephlebitis and metastatic abscesses of the liver are 
encountered. 

Colitis, aside from the specific form, dysentery, is most fre- 
quently due to irritation by fecal accumulations, and the sig- 
moid flexure is the common seat. The entire colon may, how- 
ever, be involved. Thickening of the mucous membrane and 




Fig. 237. — Ulcerative and perforative appendicitis, showing perforations ; two fecal con- 
cretions from other cases of appendicitis (modified from Bollinger). 



abundant exudation of mucus are the prominent features of the 
earlier stages ; while in the later stages atrophy and thinning are 
observed. Ulcerations are not uncommon. When the mucous 
exudation and the desquamated cells accumulate upon the surface 
the appearance of a pseudomembrane is simulated, and casts of the 
bowel or masses of mucus may be discharged from time to time 
(mucous colitis). 

Proctitis, or inflammation of the rectum, may be due to 

direct irritation by retention of fecal matter, by parasites, or by 
toxic agents ; or it may occur secondarily after various other 
diseases of the rectum, such as tumors, hemorrhoids, and the 
like. The inflammation tends to become chronic. The rectum 
is generally involved with the colon in cases of mucous colitis. 

The mucous membrane is considerably swollen, often edema- 
tous, and usually presents petechial hemorrhages. Ulceration 



DISEASES OF THE GASTR O-IXTESTIXA L TRACT. 527 



may occur secondarily, and extension of the ulcerative process to 
the surrounding tissues (periproctitis) is not unusual. In the 
latter cases fistulous communication may be established between a 
perirectal abscess and the rectum {incomplete fistula), or a fistulous 
communication may form between the rectum and the exterior 
{complete fistula in ano). Sometimes proctitis is secondary to peri- 
proctitis occurring in diseases such as typhoid fever, pyemia, and 
the like. 



INFECTIOUS DISEASES. 

Dysentery is a specific, endemic or epidemic inflammation 
of the large intestine. The term probably includes a variety of 
affections due to different causes. 

In the milder cases of endemic dysentery tainted food and 
products of fermentation, with perhaps specific bacteria, are the 
causative agents. Occasionally certain poisons, like mercury, pro- 
duce similar lesions. In cases of ulcerative dysentery, especially 
the tropical forms, the Amoeba coli is usually regarded as the 
specific cause (see Part I.). This organism probably enters the 
intestinal tract through drinking-water and multiplies in the large 
intestine, where it invades the mucosa and occasions widespread 
ulceration. Recently a bacillus has been discovered in certain 
forms of tropical dysentery. The bacillus is quite probably specific. 

The etiology of the most severe forms of dysentery remains 
obscure, but the association of certain cases with violent septic 
diseases suggests the causal factors. 

Pathologic Anatomy. — Several varieties may be distinguished, 
though one of these merges gradually into the other. 

Catarrhal dysentery is the mildest form. It is characterized 
by congestion, swelling, and edema of the mucous membrane. 
Petechial hemorrhages and follicular enlargements or ulcers are 
not unusual. 

Ulcerative dysentery is marked by swelling of the mucosa and 
scattered ulcers having a more or less irregular and ragged outline 
and undermining the mucosa, The ulcers are often surrounded 
by hemorrhagic infiltration. The ulcerative form tends to be- 
come chronic, causing great thickening of the bowel and indolent 
ulcers. 

Diphtheritic dysentery is distinguished by the presence of a 
pseudomembranous deposit in and upon the mucous membrane. 
The entire wall of the colon and rectum may be covered with a 
grayish or brownish, more or less necrotic, membrane ; or smaller 
areas of like character may be scattered here and there upon a 
thickened and catarrhal surface. In the mildest cases the process 
is entirely superficial, in the severest it extends deeply, and the 
muscularis mucosae and even the submucosa may be destroyed. 
To the most violent of all forms the term gangrenous dysentery is 
applicable. Microscopically, the epithelial cells show granular 



528 



TEXT-BOOK OF PATHOLOGY. 



degeneration and become more and more necrotic. They are 
embedded in a fibrinous or mucofibrinous matrix, and round cells 
invade the membrane as well as the subjacent tissues. 

Results of Dysentery. — In all cases there is a tendency to 
chronic thickening or inflammation of the large bowel ; and 
mucous colitis or merely a tendency to repeated acute colitis may 
remain. Occasionally perforation occurs, and peritonitis or peri- 
proctitis results. The most frequent complication is abscess of 
the liver resulting from embolism or from ascending thrombosis 
of the portal vein. In amebic dysentery the Amoeba coli is 
carried to the liver in emboli and occasions secondary changes. 

Cholera. — Cholera epidemica, or Asiatica, is an acute specific 
inflammation of the small and large intestines, due to the comma- 
bacillus orvibrion of Koch. This micro-organism is found in the 
great majority of cases. Occasionally it is not discovered, while 
other micro-organisms, Bacillus coli communis and streptococci, 
are present. It is probable that in these instances errors of obser- 
vation cause the failure of detection. 

Pathologic Anatomy. — Cholera is characterized by redness and 
swelling, and not rarely by petechial ecchymosis of the mucous 
membrane, particularly of the small intestine. The superficial 
epithelium suffers early and extensive degeneration, perhaps a 
form of coagulation-necrosis. The solitary follicles and the 
agminated glands may enlarge and may suffer ulceration. The 
intestines contain and discharge a serous exudation, often in large 
quantities, and containing grayish or whitish particles, which are 
flakes of desquamated and degenerated epithelium. The term 
" rice-water" discharges is applied to the evacuations. Exten- 
sive areas of the mucous membrane may be laid bare by the 
desquamation of the epithelium. When cholera has passed to 
its later stages secondary pseudomembranous inflammation of the 
mucous membrane is not unusual, and is probably the result of 
secondary infection. 

Associated Conditions. — The blood is thickened and dark-red in 
color ; thrombosis in the heart or venous sinuses is frequent. The 
kidneys present marked congestion and degeneration, which are 
dependent upon the action of the toxins of the disease. Lobular 
pneumonia is a common complication. 

Typhoid fever is distinguished by an acute, specific inflam- 
mation of the lymphoid elements of the intestines, particularly of 
the ileum and upper portion of the colon. The specific cause is 
the Bacillus typhi abdominalis, described by Eberth and Gaffky. 
This organism enters the gastro-intestinal tract with drinking- 
water, milk, or other food, and multiplies in the small intestine 
(see Part I.). 

Pathologic Anatomy. — The specific lesions of typhoid fever oc- 
cur in the lymphatic structures, notably in the solitary follicles, 
Peyer's patches, mesenteric glands, and spleen. 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 529 



The solitary follicles and Peyer's patches of the lower end of 
the ileum are first affected, but later, or exceptionally in the be- 
ginning, the lymphoid collections of the upper part of the ileum 
and jejunum, or of the cecum and 
colon, may be involved. At first 
the follicles and patches are swol- 
len and somewhat reddened by 
congestion. Within a few days 
of the onset, however, they lose 
their congested appearance and 
present themselves as grayish or 
white elevations projecting from 
one to several millimeters above 
the surface (Fig. 238). Micro- 
scopically the lymphoid elements 
are found in a state of active pro- 
liferation, and in addition large 
round cells (endothelial or epithe- 
lioid) are more or less abundant. 
These large cells are actively 
phagocytic, and have been dis- 
covered in the lymphatic chan- 
nels at some distance from the 
local lesions, as well as in the 
mesenteric glands, and in distant 
parts. The surrounding mucosa 
may be normal in appearance, or 
may be somewhat inflamed. The 
conditions of the lymphoid struct- 
ures at this stage, to which the term medullary infiltration has been 
applied, remain unchanged for some days or a week. After the 




Fig. 238.— Typhoid fever, showing stage 
of medullary infiltration; enlargement 
of lymphoid follicles and Peyer's patches 
(modified from Kast and Rumpel). 




Fig. 239.— Typhoid fever, showing necrosis of Pever's patches and intense congestion of 
the bowel (modified from Kast and Rumpel). 



first week necrosis is prone to occur. The center of the solitary 

34 



530 



TEXT-BOOK OF PATHOLOGY. 



follicles or part of the Peyer's patch becomes more and more soft 
and yellow, or sometimes reddish from absorption of blood-pigment. 
The necrotic portions are discharged after a few days, leaving an 
ulcerated surface of regular or irregular outline, and presenting 
necrotic edges with hemorrhagic infiltration (Fig. 239). The ul- 
cers resulting from destruction of the solitary follicles are small 
and rounded, while those involving the Peyer's patches are elon- 
gated, the long axis being parallel with the axis of the intestine. 
The ulcers are usually found in an acute stage at the end of the 
second or at the beginning of the third week of the disease. Reso- 
lution may occur without necrosis and ulceration, but more com- 
monly ulcers are formed and healing proceeds more slowly. The 
lymphoid elements of the follicles and patches are usually perma- 
nently destroyed, and healing takes place by proliferation of the 
fibrous stroma. Occasionally, however, complete restitution of 
the normal tissues occurs. When the lymphoid follicles of the 
patches have become necrotic and have been infiltrated with blood 
dark pigmented spots are formed, and give rise to the condition 
designated as the " shaven-beard " appearance. 

Complications. — Extensive necrosis may lead to erosion of a 
blood-vessel and hemorrhage ; or the wall of the intestine may be 
completely perforated by the necrotic process, and fatal peritonitis 
may result. In other instances peritonitis occurs without perfora- 
tion by direct extension of the inflammatory process through the 
intestinal wall. Very commonly slight reactive peritonitis is 
found on the serous surface opposite the ulcers. Extensive peri- 
tonitis rarely occurs in this way. Peritonitis in rare instances re- 
sults from necrosis of the mesentery glands, or from rupture of 
the spleen. 

The mesenteric glands are characteristically enlarged, those 
nearest the points of ulceration being first and most prominently 
involved. In the first stage they are soft and dark-red in color, 
•exuding a small amount of liquid on section. Later they become 
larger, harder, and of whitish appearance ; they may finally suffer 
necrosis and rupture. Usually, however, resolution takes place 
after the first stage. 

The spleen is enlarged in most cases, and presents the charac- 
teristics of acute splenic tumor. Very rarely perisplenitis or 
abscess may occur. 

Lesions in Other Parts. — The muscles, particularly those of the 
abdominal walls, frequently show spots of degeneration of a waxy 
or hyaline character, as described by Zenker. Very rarely pete- 
chial or considerable hemorrhages may be found in the muscles ; 
and abscesses are sometimes met with as sequelae. 

The heart-muscle is involved in perhaps a majority of the 
cases. The muscle-fibers suffer parenchymatous and hyaline 
degeneration ; and less commonly the intermuscular tissues pre- 
sent the characteristics of acute myocarditis. Acute endocarditis 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 



531 



and inflammations of other serous surfaces are rare in typhoid 
fever as compared with some other infectious diseases. 

Acute degeneration of the kidney and acute nephritis are quite 
common, and the kidney-substance may present small necrotic or 
lymphomatous foci. Similar lymphomata occur in the liver and 
throughout the peritoneum. 

Acute lobular pneumonia and croupous pneumonia are frequent 
complications. Osteomyelitis is rare. 

The blood in typhoid fever, unlike other infections, presents no 
leukocytosis, but, on the contrary, may be characterized by leu- 
kopenia, the mononuclear leukocytes predominating. 

Tuberculosis. — Tuberculosis of the intestines is very com- 
mon. It may occur primarily from the drinking of infected milk 
or consumption of the meat of tuberculous animals. Primary 
tuberculosis of this character is especially frequent in young in- 
fants. More commonly tuberculosis of the intestines is secondary 
to pulmonary or laryngeal tuberculosis, and is due to the swallow- 
ing of sputa. 

The usual situation of the lesions is the lower end of the ileum, 
and it is the lymphoid tissues that are prone to be attacked. At 
first the follicles or Peyer's patches become enlarged and project 
above the surface. Soon they undergo necrosis and discharge 
their contents, leaving more or less irregular caseous ulcers. The 
follicular ulcers are small and rounded, but the more characteristic 
lesion is an irregular ulcer extending transversely to the long axis 
of the bowel and often involving a half or more of the entire cir- 
cumference. These ulcers usually begin as follicular ulcers ; later 




Fig. 240.— Tubercular ulceration of the intestine. 



the submucosa is invaded and the tuberculous process extends in 
a lateral direction along the lymphatic channels running toward 
the mesentery (Fig. 240). 



532 



TEXT-BOOK OF PATHOLOGY. 



Microscopically the changes are found to involve the mucous 
membrane and the adjacent submucous coat. Early caseation is 
characteristic. On the serous coat may often be seen granular 
elevations in clusters opposite the ulcers in the mucosa, and ex- 
tending in lines from the region of ulceration around the bowel 
toward the mesentery (Fig. 241). These represent tuberculous 




Fig. 241.— Miliary tubercles in clusters and disseminated over the serosa (peritoneum) 
of the intestine ; the clusters are situated opposite ulcerations of the mucous membrane 
(modified from Bollinger). 

lymphangitis and small miliary tubercles in the course of the 
subserous lymphatic vessels. 

Tuberculous ulceration rarely causes perforation of the bowel, 
excepting in the rectum, where periproctitis and fistula in ano may 
result. The ulcers may heal, causing cicatricial distortion or 
stenosis. Very commonly there is associated tuberculous enlarge- 
ment of the mesenteric glands, and sometimes the latter are 
extensively diseased, though the primary intestinal involvement is 
insignificant. Generalized enteritis of catarrhal character may 
accompany the specific ulcerative disease. 

Syphilis is most frequent in the rectum, though cases of 
syphilitic disease of the small intestine or colon, in the form of 
localized or diffuse gummatous involvement, sometimes with 
secondary ulceration, have been observed, particularly in cases 
of congenital syphilis. 

In the rectum syphilis may appear in the form of warty eleva- 
tions or as a chancre ; also as mucous patches, gummatous nodules 
or infiltrations. Considerable thickening of the mucosa and sub- 
mucosa, with ulceration and secondary cicatrization and stenosis 
{syphilitic stricture), may result. 

Anthrax occasionally affects the small intestine in persons 
exposed to infection by their occupations. It is met with among 
wool-sorters, brushmakers, tanners, and the like. More or less 



DISEASES OF THE GASTR O-INTES TINA L TRACT. 



533 



extensive ulceration is seen in the small intestine, and sometimes 
in the large intestine. The ulcers are dark-colored and necrotic 
in appearance, and are commonly surrounded by a hemorrhagic 
zone. Considerable edema and hemorrhagic infiltration of the 
neighboring parts of the intestine may accompany the ulceration. 
The neighboring lymph-glands and the spleen are enlarged. The 
bacilli of anthrax are found in considerable numbers in the ulcers 
and in the surrounding tissues. 

Actinomycosis of the intestines is very rare. It most com- 
monly affects the region of the cecum, causing first infiltrations 
and then ulcerations of the mucosa and submucosa. 

Knteromycosis is a term applied to intestinal affections 
resulting from the ingestion of putrid meat, fish, sausages, and the 
like. Occasionally considerable epidemics may occur. The intes- 
tines may present the lesions of catarrhal enteritis or of intense 
croupous or pseudomembranous inflammation, and there may be 
erosions or ulceration. Micro-organisms of various sorts have 
been discovered, but no specific form is recognized. The acute 
general symptoms, and even the local lesions, may be caused by 
poisons elaborated by bacteria in tainted foods, rather than by the 
micro-organisms themselves. 

TUMORS. 

Connective-tissue Tumors. — Among the benign tumors of 
the intestines fibroma, myxoma, and lipoma are occasionally met 
with in the submucosa as small nodular tumors or as pendulous 
polyps. They may occasion intestinal obstruction and even invag- 
ination. 

Sarcoma of the intestine is rare. Lymphosarcomatous or lym- 
phadenomatous enlargement of the solitary follicles or Peyer's 
patches may be met with in leukemia or pseudoleukemia. Round- 
celled sarcoma springing from the submucosa and deeper layers 
of the mucosa, and sometimes infiltrating the mesentery, may also 
occur as an independent and primary affection. Nodules of 
secondary sarcoma are not rarely met with in the mucosa and 
submucosa of the intestines (Fig. 242), and the serous covering 
may be studded with miliary nodules in sarcomatosis. 

Epithelial Tumors. — Among the epithelial tumors may be 
included inflammatory papilloma, adenoma, and carcinoma. 

Inflammatory hyperplasia of the mucous membrane may occur 
in association with chronic inflammations, especially in the large 
intestine, and may lead to the formation of papillomatous or poly- 
poid elevations of considerable magnitude. 

Adenomata are more strictly of the nature of tumors, being 
independent of inflammatory processes, although no sharp dividing- 
line can be drawn between the inflammatory proliferations and the 



534 



TEXT-BOOK OF PATHOLOGY. 



adenomata proper. The latter may occur in the form of flat ele- 
vations having a more or less uneven surface and a tendency to 




Fig. 242.— Nodule of secondary sarcoma in the mucosa of the intestine (Kast and Rumpel). 

hemorrhage and ulceration ; or in the form of papillomatous 
elevations of a cauliflower character. Adenomata arise by 




Fig. 243.— Carcinoma of the duodenal papilla (modified from Kast and Rumpel). 

hyperplasia of the crypts of Lieberkiihn in the duodenum or of 
Miiller's glands, and in their structure they present typical gland- 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 535 



ular acini, the tubules having a basement-membrane lined with 
cylindrical epithelium. Adenomata are most frequent in the rec- 
tum, but may occur in other parts of the large intestine and in 
the duodenum. 

Carcinoma is the most frequent tumor of the intestines. It 
occurs in the duodenum, especially at the papilla of the common 
bile-duct (Fig. 243) ; at the ileocecal valve, at the flexures of the 
colon, and in the upper or lower part of the rectum. The appear- 
ance is that of a soft, irregular, often ulcerated and bleeding ele- 
vation, projecting into the lumen of the gut and causing considerable 
narrowing, or surrounding the bowel by circular involvement of the 
entire circumference. The carcinomata of the bowel are, for the 
most part, cylindrical epitheliomata (Fig. 244) or glandular can- 




Fig. 244.— Cylindrical epithelioma of the intestine (Perls). 



cers, consisting of atypical acini and tubules, with irregular prolif- 
eration and infiltration of the neighboring tissues with masses of 
epithelial cells. Cases are met with, especially in the rectum, in 
which there is a clear transition of adenoma into carcinoma (adeno- 
carcinoma), and in general adenomata of the bowel have a tendency 
to such transformation (Fig. 245). At the lower end of the rectum 
squamous epithelioma may occur. 

The results of carcinoma of the bowel are the same as those of 
stenosis due to other causes, together with the consequences of the 
cancerous cachexia and of metastasis. Ulceration of the tumor 
may lead to perforation. 

Myoma of the intestines and multiple cysts are occasionally met 
with. 



536 



TEXT-BOOK OF PATHOLOGY. 




PARASITES. 

Vegetable Parasites. — Various forms of bacteria are found 
with such frequency in the intestinal contents that it is difficult to 
estimate their pathologic significance. Tubercle-bacilli, the bacil- 
lus of glanders and of typhoid fever, and the actinomyces produce 
the specific lesions of these diseases. The Bacillus coli communis 
is a constant inhabitant, but probably assumes pathogenic proper- 
ties and leads to inflammatory lesions when the conditions (such as 
irritation by coarse food, congestion, obstruction) favor its activity 
and multiplication. Under the same circumstances other micro- 
organisms likewise become active in the production of enteritis. 

Animal Parasites. — The animal parasites are discussed in 
detail elsewhere, but may be briefly mentioned here with reference 
to pathologic results occasioned by their presence. Various forms 
of protozoa have been found, and may occasion inflammations 
when in considerable numbers. Coccidial psorospermia occur in 
the epithelium of the villi of the small intestine, and the Megalos- 
toma entericum may be found attached to the epithelium. The 
Amoeba coli may lie free in the contents, or may penetrate through 
ulcerations. It inhabits the large intestine, and is the probable 
cause of certain kinds of dysentery. 



DISEASES OF THE GASTROINTESTINAL TRACT. 537 



The larger intestinal parasites are, for the most part, species of 
vermes. Among the tape-worms Taenia saginata, Taenia solium, 
and Bothriocephalus latus are the most frequent. Occasionally 
these may lead to intestinal obstruction by forming thick knots or 
coils, and sometimes the head of the worm may be attached in the 
mouth of the bile-duct, causing obstruction and jaundice. Inflam- 
matory changes are rarely met with as a result of these worms. 

Among the nematodes, or round worms, the Ascaris lumbri- 
coides, or ordinary round worm, is the most frequent. It is usu- 
ally multiple, and may occasion obstruction of the intestine or 
inflammation. Sometimes they perforate the intestinal wall, but 
it is improbable that the perforation is due entirely to the action 
of the worm. Previous intestinal ulceration is the more import- 
ant condition. Obstruction of the bile-ducts or of the appendix 
may occasionally be due to 'lumbricoids. The Ankylostoma du- 
odenalis may cause petechial hemorrhages and inflammatory dis- 
turbances in the duodenum or jejunum. The worms attach them- 
selves firmly to the mucous surface and may be present in large 
numbers. The Oxyuris vermicularis, or thread-worm, occupies 
the large bowel, multiplying in the cecum and descending in the 
mature state to the rectum ; it may occasion considerable proctitis. 
In female children vaginitis sometimes results from migration 
of the worms. The Trichina spiralis when ingested in large 
numbers occasions violent gastro-enteritis, and its embryos per- 
forate the wall of the intestine and migrate to the muscles. 

Larvae of various forms of flies occasionally occupy the intes- 
tinal tract, and owe their presence to the ingestion of the eggs 
with food. They may occasion enteritis, and may be found in 
immense numbers in the bowel or the stools. 

INTESTINAL RUPTURE AND FOREIGN BODIES. 

Rupture may be due directly to traumatism or penetrating 
wounds ; but more frequently results from ulcerations within. 
Duodenal (peptic) ulcers not infrequently perforate, and typhoid 
ulcers occasionally cause rupture. Tubercular, dysenteric, and 
other ulcers are less prone to penetrate completely. The appen- 
dix may rupture from obstruction at its mouth and secondary 
catarrhal, necrotic, or gangrenous inflammation of its walls. Rec- 
tal ulcers frequently cause painful diarrhea, proctitis, periproctitis, 
and fistulae. 

Intestinal rupture usually leads to rapid peritonitis, but occa- 
sionally recovery ensues. A localized peritonitis, by walling off 
the infected area, may prevent general infection. The rupture 
may take place between contiguous coils, causing spontaneous in- 
testinal anastomosis. 

Foreign-bodies. — Various bodies that have been swallowed 



538 



TEXT-BOOK OF PATHOLOGY. 



may lodge in the intestines. Occasionally fecal concretions or 
enteroliths are found, especially in the appendix. These con- 
sist of a nucleus of epithelial cells, mucus, hair, and the like, sur- 
rounded by inspissated fecal matter and earthy salts, phosphate of 
lime and carbonate of calcium. They may cause considerable 
irritation, especially in the appendix, and even perforation. 

THE LIVER. 

Anatomic Considerations. — The liver is peculiar in hav- 
ing a double circulation ; one system of vessels, the portal 
vein and its ultimate subdivision, receiving the blood from the 
digestive tract for functional purposes ; the other system, the 
hepatic artery and its branches, supplying the nutritive blood 
for the walls of the blood-vessels and for the interlobular con- 
nective tissues, as well as to a certain extent the proper hepatic 
structure itself. The portal capillaries ramify through the acini 
and empty into small branches of the hepatic vein lying in the 
center of the acini. The capillaries of the hepatic artery traverse 
the interlobular tissue and ultimately empty into the interlobular 
branches of the hepatic vein. The primary biliary capillaries are 
merely spaces between the hepatic cells, the larger formed capil- 
laries occupying the interlobular tissues. 

MALFORMATIONS AND CHANGES OF POSITION. 

Congenital malformations are uncommon. There may be 
complete absence of the organ, especially in certain monstrosities ; 
more frequently adventitious hepatic tissue is found in the suspen- 
sory ligament or elsewhere. Minor abnormalities in the lobes or 
fissures are more frequent. Absence of the gall-bladder and con- 
genital stenosis or occlusion of the hepatic ducts are occasionally met 
with. 

Congenital Alterations of Position. — The liver may 
occupy the left side in transposition of the viscera. More rarely 
it is displaced downward, or occupies other abnormal positions. 

Acquired Changes of Form. — The most important of 
these is contraction and lengthening of the organ by lacing. 
This gives rise to compression along the line of the lower mar- 
gin of the ribs ; the right lobe of the liver may thus be divided 
into an upper and a lower portion by a deep fissure. The capsule 
is frequently thickened and the superficial acini atrophic at the 
line of constriction. Similar indentation by the ribs posteriorly, 
or by the right eras of the diaphragm, results from pulmonary 
affections and enlargements of the liver. Other changes of form, 
due to special diseases of the liver, will be discussed below. 

Acquired Changes of Position. — Downward displacement 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 539 



may result from pleural effusion or emphysema ; or it may be due 
to relaxation and lengthening of the suspensory ligaments. The 
latter form is more common in women than in men, and is often 
part of a general enteroptosis. Tight lacing may be a cause of 
importance. Displacement to the right or left, or tilting upward 
of the lower edge, may occur in association with various abdominal 
and thoracic affections. 

CIRCULATORY DISTURBANCES. 

Anemia of the liver may be part of a general anemia, or it 
may be due to pressure upon the organ, to various diseases of the 
liver-substance, or to compression of the blood-vessels. The sub- 
stance becomes pale and, if the anemia persists, undergoes degen- 
eration. 

Active hyperemia is physiologic during digestion, and 
occurs in association with various inflammatory abdominal dis- 
eases. It is rarely extensive, and does not lead to marked 
pathologic changes. 

Passive hyperemia results from obstruction to the circula- 
tion due to cardiac or pulmonary diseases, to pleural effusion or 
adhesions, or to thrombosis or compression of the upper part of 
the inferior vena cava. It is especially characteristic of cardiac 
affections, the sluggish venous circulation of the liver accounting 
for the fact that this organ first evidences failing cardiac power. 

The liver increases in size, often considerably ; the edges are 
rounded, and the color on the surface is darker than normal. On 
section there may be seen deeply congested central veins sur- 
rounded by lighter areas, representing the substance of the acini. 
If the process has persisted, secondary fatty degeneration of the 
peripheral zones of the acini or atrophy of these takes place, and 
the light color of such portions, contrasting strongly with the dark, 
congested central vein, suggests the name nutmeg-liver (Fig. 246). 
In some instances of intense congestion small hemorrhages may 
occur, especially in the portions lying beneath the capsule. In 
the later stages degeneration and reduction of size may take 
place and the organ may become dark-red from deposit of hema- 
togenous pigment. To this form the term red-atrophy is some- 
times given. In other instances hyperplasia of the connective 
tissues between the lobules and acini occurs, while at the same 
time the organ is darkly pigmented. The term cyanotic indu- 
ration may appropriately be given to such. Cases of this sort 
are in reality instances of secondary cirrhosis. 

Passive congestion of the liver may occasion considerable dis- 
turbance of the hepatic function. The most striking evidence of 
this is jaundice. This is probably due to the compression of the 
smaller biliary ducts and capillaries, and in part to swelling of 



540 



TEXT-BOOK OF PATHOLOGY. 



the lining cells of these channels. The bile at the same time is 
probably thicker than normal, and does not therefore as readily 
escape through the ducts as in health. 




Fig. 246.— Nutmeg liver : chronic congestion due to cardiac disease (Bollinger). 

Embolism and thrombosis of the portal vein may occur in 
consequence of various diseases of the gastro-intestinal tract, par- 
ticularly in cases of ulcerative enteritis. Embolic occlusion of 
one of the larger branches of the portal vein may occasion no 
serious circulatory disturbances, on account of the free collateral 
circulation and from the fact that the hepatic artery is capable of 
supplying the entire hepatic circulation. Embolic or thrombotic 
occlusion of the branches of the hepatic artery is similarly devoid 
of serious disturbance of the circulation. 

Obstruction of the interlobular branches of the portal vein, 
and particularly when several are coincidently occluded, may 
occasion decided nutritive disturbances in the hepatic acini. 
Small areas of necrosis having a grayish or yellowish and some- 
what granular appearance, or in other cases foci of necrosis with 
hemorrhagic infiltration, are the striking lesions. Such conditions 
are observed in most instances of death from puerperal eclampsia 



DISEASES OF THE GASTR O-INTESTINA L TRACT. 541 



in consequence of thrombosis or of embolism of decidual cells 
(Fig. 247), and in consequence of various intoxications or infec- 
tions having their origin in the distribution of the portal circula- 
tion. The immediate cause of the lesions in the latter conditions 
is hyaline thrombosis of the interlobular portal vessels. 





•'5 #V 


s, 




* * * * . 




i _ 


\ * < ■ 5 


- * * • * " 



Fig. 247.— Coagulation-necrosis of the hepatic cells in a case of puerperal eclampsia 

(Karg and Schmorl). 

Thrombosis of the portal vein is most frequently the result of 
infective inflammation of the vein (pylephlebitis), resulting from 
ulcerative enteritis, appendicitis, or similar processes involving 
the parts from which the portal blood is received. There may 
be a gradual ascending inflammation and thrombosis extending 
from the primary focus of disease to the portal vein ; or the 
latter may be involved in a more direct manner by infectious 
embolism. The portal vein and its branches in the liver become 
more or less obstructed, and serious disease of the liver may 
occur (multiple abscesses). At the same time the obstruction of 
the vein occasions intense passive hyperemia of the peritoneum, 
and ascites results. 

ATROPHY AND DEGENERATIONS. 

Atrophy of the liver occurs in cases of death from inanition 
or from various organic diseases. (Pressure-atrophy has been 
referred to above. Acute yellow atrophy is described below.) 

The greater part of the liver-structure may be affected, or the 
atrophy may be limited to the edges or other limited portions. 
The liver is more or less uneven, and may at the same time be 
somewhat pigmented. 

Microscopically the liver-cells are decreased in size, granular, 
and dark-colored. At times the acini may disappear entirely, 
and reactive hyperplasia of the stroma and even proliferation of 
biliary ducts may ensue. 



542 



TEXT-BOOK OF PATHOLOGY. 



Localized atrophy occurs in the vicinity of tumors, in the acini 
surrounded by hyperplastic connective tissue in cirrhosis, and in 
parts of the liver otherwise subjected to pressure. The liver-cells 
of the affected part become distorted and decreased in size, and 
are deeply pigmented (see Fig. 258). In the later stages they 
break down completely, and are removed. Red atrophy (see 
Congestion of the Liver) is a form of pressure-atrophy with 
pigmentation, the compression of the hepatic cells being due to 
overdistention of the hepatic veins and capillaries. 

Pigmentation of the liver is prone to occur on account of the 
sluggish circulation through that organ, and maybe of various kinds : 

1. Hematogenous pigmentation (hemachromatosis) in the portal 
areas. Particles of altered blood-pigment are often deposited 
in the interlobular tissues, especially in Kupfer's stellate cells, 
or in the peripheral zones of the acini in cases of abnormal 
blood-obstruction in the portal circulation. This is particularly 
common in pernicious anemia. In this disease the peripheral 
zones of the acini are habitually infiltrated with pigment-matter, 
which responds to tests for iron, such as with ammonium sulphid 
or ferrocyanid of potassium and hydrochloric acid. Somewhat 
similar pigmentation of the liver may occur in cases of absorp- 
tion of hemorrhagic effusions in the peritoneum, or in consequence 
of other forms of blood-destruction. Analogous pigmentation is 
often met with in the livers and other abdominal organs of 
drunkards. 

2. Hematogenous pigmentation of the central portions of the 
acini has been noted in connection with a red atrophy of the liver 
consequent upon congestion. 

3. Biliary pigmentation results from obstruction of the biliary 
ducts, and is constantly met with in certain forms of cirrhosis and 
in the vicinity of new growths which compress the biliary passages. 

4. Very rarely anthracotic pigmentation has been observed. 
In one case, at least, there was associated cirrhosis. 

Fatty infiltration is more or less physiologic, especially in 
children and in overfed individuals. Pathologically there may be 
diffuse infiltration or deposit in the liver-cells of all parts of the 
organ. Such pathologic fatty-liver may result from overeating 
and general obesity, or may be due to pulmonary disease or anemic 
and cachectic conditions. It has generally been held that the im- 
mediate cause is retarded oxidation, in consequence of which fat 
accumulates. It is probable, however, that there is some disease 
of the hepatic cells, rendering them more active in the storing up, 
or less active in disposing of fats. This seems especially true in 
certain cases due to poisons which cause a deposit of fat in the 
liver, as in geese pampered by antimonial poisoning. 

The liver increases in size, often considerably ; its edges are 
rounded, its consistency is doughy, and the color is rather yellow- 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 543 



ish and glistening. On section there may be visible exudation of 
oil-drops and the knife may be covered with droplets. 

Microscopically the process is found to begin in the peripheral 
portions of the acini in the form of droplets within the hepatic 
cells. Soon these increase in size by confluence, adjacent cells are 
involved, and the entire acinus eventually becomes affected (Fig. 
248). In extreme cases the hepatic cell is filled with a single 




Fig. 248— Fatty infiltration of the liver. 



large oil-drop, which compresses the protoplasm and nucleus. 
The blood-vessels and other structures may be completely hidden 
from view ; and the pressure of the fatty deposit may be sufficient 
to produce a certain degree of anemia, though not enough to occa- 
sion serious circulatory disturbances. The functional activity of 
the liver is diminished. 

Parenchymatous degeneration, or cloudy swelling, occurs 
in various infectious fevers and in consequence of intoxications, 
notably by phosphorus, arsenic, and antimony. The liver is some- 
what enlarged, and of an opaque, grayish-yellow appearance, the 
outlines of the lobules being extinguished. Microscopically, the 
liver-cells are found filled with fine albuminous granules more or 
less obscuring the nucleus. In most instances cloudy swelling 
terminates by return to the normal state ; but if the intoxication 
or infection is continued, fatty degeneration may result. 

Fatty degeneration may occur as the result of severe 
anemia, particularly pernicious anemia, or, following cloudy 
swelling, as the result of infectious diseases or of intoxications. 
Among the infections, pyemia, yellow fever, relapsing fever, 
and erysipelas are notable examples. The liver may be greatly 
decreased in size and softer than normal ; the substance not rarely 
is friable. The color is yellowish, and oil-drops may exude from 



544 



TEXT-BOOK OF PATHOLOGY. 



the surface. Microscopically the hepatic cells are filled with 
small granular particles or droplets of fat, and in the advanced 
stages they break down completely into granular detritus. Fatty 
degeneration of localized areas of the liver or of individual acini 
or cells occurs in association with chronic hepatitis or other dis- 
eases causing pressure upon the acini. 

Acute Yellow Atrophy. — The most advanced fatty degen- 
eration of the liver occurs in the affection of the organ termed 
acute yellow atrophy. This condition is most frequent in young 
women, and especially in those addicted to the excessive use 
of alcohol. Occasionally syphilis seems the etiologic factor, and 
in some instances of phosphorus-poisoning the appearance of the 
liver is the same as that which is recognized as acute yellow 
atrophy. Finally, some cases are idiopathic, arising without 
recognizable cause. Parturition seems a determining cause in 
some cases. Micro-organisms of various kinds have been found, 
and it is likely that all cases are toxic or infectious. 

Pathologic Anatomy. — The liver is decreased in size and be- 
comes remarkably soft and friable. On section there is found a 
variegated appearance, the prevailing color being a brownish or 
grayish-yellow, in which are scattered bright or dark-red areas. 
The yellowish areas represent the degenerated and pigmented 
hepatic cells ; the reddish areas foci of hemorrhagic infiltration or 




Fig. 249— Acute yellow atrophy of the liver, showing extensive fatty degeneration and in 
places complete destruction of the liver-cells (Kast and Rumpel). 



pigmentation. The process usually begins in the left lobe, but 
rapidly involves the entire organ. Sometimes the liver is in- 
creased in size during the initial stages, and occasionally a liver 
enlarged by previous disease suffers terminal acute atrophy. 

Microscopically the hepatic cells are found to have undergone 
rapid fatty degeneration or necrosis, and are filled with or replaced 
by yellowish pigment-particles. As the process advances, the cells 
are completely destroyed (Fig. 249). In the red areas referred to, 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. 545 

infiltration with blood-cells and hematogenous pigmentation are 
observed. 

Associated Conditions. — Acute yellow atrophy leads to intense 
cholemia, in consequence of which biliary pigmentation of the 
various structures of the body may develop. Petechial hemor- 
rhages may occur in the mucous or serous membranes, or in the 
skin. The urine contains leucin and tyrosin. More or less pro- 
found acid intoxication may occur (see Acid Intoxication, Part I.). 

Amyloid degeneration occurs in consequence of syphilis, 
tuberculosis, and suppurative diseases of the bones, or as a re- 
sult of long-standing cachexia. It is habitually associated with 
amyloid disease of the spleen, and often of the kidneys and other 
structures. 

Amyloid degeneration begins in the smallest blood-vessels 
between and within the acini, causing a more or less pronounced 
thickening of their walls. The liver-cells themselves may be 




Fig. 250.— Amyloid liver (from a photograph by Dr. Wm. M. Gray). 

secondarily involved, but more frequently undergo atrophy and 
fatty degeneration in consequence of the pressure and of dimin- 
ished nutrition due to compression of the blood-vessels (Fig. 250). 

The liver is enlarged and denser than normal. Not rarely it 
presents a striking translucency, and on section the color is gray- 
ish-white or yellow. The peripheral ard central zones of the 
acini are sometimes readily distinguished by their light color from 
the innermost portions, which are least affected. 

Dropsical infiltration of the liver-cells occurs in cases of 
intense infection and intoxication, especially such as originate in 
some part of the portal circulation. It is found particularly in 
the vicinity of necrotic areas due to embolic occlusion of the inter- 
lobular portal veins. The liver-substance is swollen, and micro- 
scopically the cells are cloudy and ofttimes vacuolated. 



35 



546 



TEXT-BOOK OF PATHOLOGY. 



INFLAMMATIONS. 

Hepatitis, or inflammation of the liver, may be of several 
forms : a parenchymatous, an acute interstitial, or a chronic inter- 
stitial. 

Parenchymatous Hepatitis. — In the course of various 
infections and intoxications a certain amount of parenchymatous 
degeneration of the liver-cells may take place. This was for- 
merly described under the name parenchymatous hepatitis. The 
term is generally inappropriate, though in some instances there is 
associated with the degeneration of the hepatic cells a certain 
amount of cellular infiltration and reactive inflammation. To 
such cases the term parenchymatous inflammation might be ap- 
plied, though in reality even these are more degenerative than 
inflammatory in nature. 

Acute Interstitial Hepatitis, or Abscess of the I4ver. 
— In practically all, if not all, cases abscess of the liver is due to 
the action of micro-organisms. The bacteria may gain access in 
several ways. In some cases penetrating wounds, or perforation 
of gastric or duodenal ulcers or of other pathologic lesions into 
the liver, occasion direct infection. In other cases the micro- 
organisms are carried in the circulation and enter the liver with 
the portal or hepatic blood, or by retrograde embolism through 
the hepatic veins from the vena cava. Finally, infection may 
occur by invasion of the bacteria along the bile-ducts. 

Most frequently hepatic abscess is secondary to ulcerative dis- 
ease of the intestines, notably dysentery. In this disease the 
specific amebre are carried to the liver in the portal circulation, 
and occasion necrotic foci in which the bacteria carried within the 
amebse multiply and give rise to the further changes constituting 
an abscess. Similar embolic abscesses occasionally follow appen- 
dicitis and perityphlitis, or various forms of intestinal ulceration. 
Thrombophlebitis of the portal vein not rarely extends to the 
smaller branches within the liver, and occasions multiple suppu- 
rative foci. 

In cases of general pyemia multiple abscesses of the liver may 
occur, especially when the primary infection occurs within the 
abdomen. Infection by invasion along the biliary tract is espe- 
cially prone to occur when there is obstruction of the bile-ducts 
by calculi or otherwise. In tropical countries traumatism without 
visible contusion may lead to abscesses, and it is not unlikely that 
micro-organisms from the biliary passages penetrate the hepatic 
structure in the injured portions. 

Among the micro-organisms that have been discovered are 
the streptococci and staphylococci, the Bacillus coli communis, 
and others less frequently. 

Pathologic Anatomy. — Dysenteric and traumatic abscesses are 



DISEASES OF THE GA STB O-INTESTINA L TRACT. 547 



usually solitary, and generally occupy the right lobe. In the 
early stages they appear as spots of grayish or yellowish color, in 
which the division of the lobules is lost and which assume a more 
and more granular appearance. Subsequently softening takes 
place, and a cavity is formed. This increases in size until in ad- 
vanced cases it may reach enormous proportions. The contents 
consist of curdy or creamy pus having a yellowish, brownish, or 
often quite reddish appearance, and the wall is composed of an ill- 
formed pyogenic membrane. The abscess may consist of a single 
cavity, or may be partially lobulated. Sometimes there are mul- 
tiple abscesses. If the cavity is small, resorption of the pus may 
take place and a cicatrix may result. In other cases inspissation 
and encapsulation ensue. Large abscesses may rupture into the 
pleura, into the stomach or intestines, into the peritoneal cavity, 
or externally. Not rarely the diaphragm and lungs are penetrated, 
and the pus is evacuated through the bronchi. 

Metastatic abscesses, and those due to infection from the biliary 
ducts or to suppurative pylephlebitis, are multiple and usually of 
small size. 

Chronic interstitial hepatitis, or cirrhosis of the liver, 
is a form of diffuse hyperplasia of the connective tissue, beginning 
in the interlobular tissues and sometimes extending into the acini, 
or causing secondary changes in the liver-cells. Hyperplasia of 
the interlobular bile-ducts, and less frequently of the hepatic cells, 
may be observed. 

Etiology. — Cirrhosis of the liver is essentially the result of 
hematogenous irritation. The most frequent cause is alcohol, 
and it is particularly frequent in persons who consume raw spirits. 
Overeating, with a sedentary life and a gouty diathesis, may also 
contribute. Other cases are secondary to infectious diseases, 
notably to syphilis, malaria, or tuberculosis. 

Occasionally cirrhosis is due to the absorption of irritants 
by the portal radicles and their transference to the liver in cases 
of chronic peritonitis. Certain cases are due to chronic con- 
gestion of the hepatic circulation in consequence of cardiac or pul- 
monary disease ; and, finally, obstruction of the bile-ducts may 
lead to another group of cases. Recently, certain observers have 
ascribed cirrhosis to the action of bacteria entering the portal 
circulation from the intestines. Organisms resembling the bacil- 
lus coli and its degeneration-forms have been discovered in the 
hepatic cells. 

Morbid Anatomy. — Several varieties having rather marked dif- 
ferences in their macroscopic and even microscopic appearances 
may be distinguished. The process is essentially the same in 
the different forms and the causes are similar. The most promi- 
nent varieties are atrophic cirrhosis, hypertrophic cirrhosis, and 
biliary cirrhosis. 



548 



TEXT-BOOK OF PATHOLOGY. 



Atrophic cirrhosis (Laennec's cirrhosis) is the ordinary form, 
which is also known by the name " Gin-drinker's liver." In the 
earliest stages the liver is often enlarged, but in the typical ad- 
vanced form it is contracted, extremely hard, granular, or irregu- 
larly uneven on the surface, and on section resistant to the knife 
(Fig. 251). The size of the liver, even in advanced stages, is by 
no means always small. A study of statistics obtained at the post- 
mortem table shows that the liver in perhaps a majority of the 
cases of otherwise typical Laennec's cirrhosis is larger than the 



Fig. 251. — Atrophic cirrhosis of the liver of a boy aged sixteen years, showing also thick- 
ening of the capsule and ligaments (perihepatitis). 

normal organ. The surface of section presents bands of connec- 
tive tissue surrounding groups of acini, and compressing them so 
that they rise above the surface. The connective-tissue bands are 
dull gray or white in appearance, the enclosed acini yellowish or 
brownish. 

Microscopically the process is found to begin as a proliferation 
of the connective tissues around the interlobular branches of the 
portal vein. In the earlier stage there are found round-cell infil- 
tration and proliferation of fibroblastic cells, causing moderate 
obstruction to the portal circulation. Later the connective tissue 
becomes sclerotic, greater compression of the portal veins en- 
sues, and considerable obstruction of the circulation results. At 
the same time the acini are compressed and may suffer degenera- 
tion. This, however, is rarely pronounced. There is little ten- 
dency to extensive invasion of the acini themselves by the inflam- 
matory process. New-formed biliary ducts may be present in 
considerable numbers in the hyperplastic interlobular tissue. 

Associated Changes. — The marked result of atrophic cirrhosis 



DISEASES OF THE GASTROINTESTINAL TRACT 549 



is obstruction to the portal circulation. This occasions congestion 
of the spleen and gastro-intestinal mucosa, and eventually ascites. 
When the obstruction becomes extreme collateral circulation may 
relieve the congestion of the portal system. The most prominent 
anastomoses are those between the gastric and esophageal veins, 
and between the hemorrhoidal veins and the veins of Retzius with 
the retroperitoneal veins. The veins of the round ligament 
increase in size and communicate with the superficial veins at the 
umbilicus. 

Gastro-intestinal catarrh and enlargement of the spleen are 
usually prominent in cirrhosis. Jaundice is rare, because the bile- 
ducts are rarely compressed. 

In some instances the liver is large and smoother, softer and 
lighter in color, from the fact that considerable fatty infiltration 
of the acini is associated with the cirrhosis (Fig. 252). In the 




Fig. 252.— Cirrhosis of the liver, showing new-formed connective tissue, proliferated bile- 
ducts, and fatty infiltration of some of the hepatic cells. 

later stages such cases may become converted into the typical 
form by absorption of the fat. 

Pathologic Physiology. — Cirrhosis of the liver occasions gastro- 
intestinal symptoms by obstructing the portal circulation, and 
probably also by altering the functional action of the liver. Meta- 
bolic disorders of some sort also result from the hepatic disease, 
but the nature of these is as yet unknown. The fatal termination 
often comes in the form of sudden or gradual coma, which is 
probably toxemic. 

Hypertrophic cirrhosis is perhaps more frequent in warm 
climates than elsewhere. The liver is uniformly enlarged, smooth, 
or moderately granular on the surface, and indurated. On section 
the color is seen to be more or less yellowish or greenish, and either 
uniform or mottled. 



550' 



TEXT-BOOK OF PATHOLOGY. 



Microscopically proliferation in the interlobular connective 
tissues is found, as in the atrophic form, but it does not bear the 
same relation to the portal veins and is less prone to cicatricial 
contraction. Unlike the atrophic form, there is decided extension 
into the peripheral zones of the acini, and everywhere between the 
columns of hepatic cells there may be seen proliferated fibroblastic 
cells. Within the new-formed connective tissue may be seen 
columns of low cylindrical cells surrounding a narrow canal. 
These are proliferated bile-ducts. Proliferation of the liver-cells 
themselves is also frequent, and throughout the organ the cells are 
found more or less deeply stained with biliary pigment. 

Associated Changes. — The most prominent is jaundice. Ob- 
struction of the portal circulation rarely becomes marked. 

Biliary cirrhosis is a form of chronic hepatitis consequent 
upon obstruction of the biliary ducts. The first effect of such 
obstruction is a swelling of the liver, due to the retention of bile, 
and perhaps also to congestion. Eventually the stagnation of the 
bile, with production of irritant substances, leads to reactive in- 
flammation. 




Fig. 253. — Perihepatitis associated with cirrhosis of the liver. 

The appearance of the liver is much the same as that seen in 
hypertrophic cirrhosis of the ordinary type. The organ is uni- 
formly enlarged, and may be somewhat granular upon the surface 
or entirely smooth. On section the substance is found to be 
deeply bile-stained, and has a yellowish or greenish color. The 
substance is firm, and the overgrowth of connective tissue may be 
visible on the surface. 

Microscopically the first discoverable changes are spots of in- 
sular necrosis in the peripheral zones of the acini. Subsequently 
proliferation of connective tissue replaces these and spreads to the 



DISEASES OF THE G ASTRO-INTESTINAL TRACT. * 551 



interlobular tissues. Proliferation around the interlobular biliary 
capillaries (j)erianc/iochoUtis) may be a striking characteristic from 
the first, and multiplication of new bile-ducts and of hepatic cells 
is frequently observed. In cases of absolute obstruction of the 
gall-ducts, and in cases in which active fermentative changes in 
the bile have occurred, rapid fatty degeneration and acute atrophy 
of the liver may be the terminal change. 

Perihepatitis. — Inflammation of the capsule of the liver and 
of the superficial portions of the hepatic structure may be asso- 
ciated with cirrhosis (Fig. 253), and not rarely occurs in conse- 
quence of chronic peritonitis. It may lead to considerable thick- 
ening of the capsule. The pressure of the contracting fibrous 
tissue may occasion atrophy of the underlying hepatic substance, 
and a more or less uneven and atrophic organ results. Primary 
inflammation of the capsule may be an expression of syphilitic 
infection, and may occur alone or in association with thickening 
of the peritoneum. Reference will be made, in the discussion of 
diseases of the peritoneum, to a special form of hyperplastic peri- 
hepatitis — that known as the Zuckergussleber of Curschmann. 

HYPERTROPHY. 

The regeneration after injuries of the liver shows the power of 
the liver-cells to undergo active multiplication. Not rarely active 
hyperplasia of liver-cells throughout the entire organ may occur 
in association with other diseases, notably hypertrophic cirrhosis. 
A simple hypertrophy of the liver also occurs in certain well- 
developed, robust individuals. Enlargements of the liver for- 
merly regarded as hypertrophies are, for the most part, due to 
pathologic conditions. 

RUPTURE OF THE LIVER. 

Rupture may occur from direct traumatic injury, and is par- 
ticularly common in the new-born when forcible delivery has been 
necessary. In the latter cases small injuries with secondary hem- 
orrhagic infiltration are observed near the surface of the organ. 
Portions of liver-cells may be loosened and may be carried as 
emboli to the lungs. The injury is repaired by active hyperplasia 
of the liver-cells and of the biliary capillaries, and in this manner 
the affected part may be restored without the development of scar- 
tissue. Large injuries, however, occasion the formation of cica- 
tricial tissue. 

INFECTIOUS DISEASES. 

Tuberculosis may occur in the form of minute, translucent, 
miliary tubercles, which may be scarcely visible to the naked eye 
(Fig. 254), or in the form of larger foci. Tuberculosis of the liver 
is always a secondary disease. The tubercles arise in the inter- 



552 



TEXT-BOOK OF PATHOLOGY. 



lobular tissue or from the acini themselves. The larger caseous 
tubercles are rare ; they may be associated with diffuse cirrhotic 
contraction of the organ. Miliary tuberculosis of the capsule of 
the liver not rarely occurs in tuberculous peritonitis. 




Fig. 254.— Miliary tubercles in the liver. 



Syphilis is met with in the form of diffuse infiltration and 
cirrhosis, or in the form of gummata. Either of these varieties 
may be found as a result of acquired or of hereditary syphilis. 




Fig. 255.— Syphilitic cirrhosis of the liver : lobulated liver (Kast and Rumpel). 

In the diffuse form the liver presents much the same appear- 
ances as in atrophic cirrhosis, but the connective-tissue bands 
are much more pronounced and the liver is prone to be irregu- 



DISEASES OF THE G ASTRO-INTESTINAL TRACT 553 



larly contracted and tabulated (Fig. 255). Gummata may occur 
in any part of the organ, and may be single or multiple, pre- 
senting themselves as rounded, yellowish, or grayish masses, 
ofttimes showing central necrosis and surrounded by connective- 
tissue hyperplasia (Fig. 104). Complete cicatrization may lead to 
decided scar-formation. In addition to these forms, congenital 
syphilis may manifest itself in the form of a uniform, diffuse con- 
nective-tissue hyperplasia and round-cell infiltration. The liver- 
cells are pushed apart and are ill-developed or atrophic (Fig. 256). 




Fig. 256.— Diffuse congenital syphilis of the liver. 



I/eprosy occasionally affects the liver, causing the formation 
of nodular masses. 

TUMORS. 

Fibromata, lipomata, and myomata are occasionally 
observed as nodular masses, but have little significance. 

Angioma is a more important form. This tumor occurs upon 
the surface of the organ, and is usually of small size, rarely 
exceeding that of a walnut. It is more commonly found in 
persons who have died at advanced years than in young persons. 
Angiomata appear as dark-red or bluish, slightly elevated areas, 
either sharply outlined and encapsulated, or merging gradually 
into the surrounding tissue. Microscopically they are found to be 
cavernous angiomata, and doubtless owe their origin to dilatation 
of the capillaries, with coincident atrophy of the liver-cells. 

Sarcoma of the liver may occasionally be primary, but is ex- 
ceedingly rare. Secondary sarcoma, on the other hand, is very 
common, especially the melanotic form following primary sarcoma 
of the eye. 

I/ymphadenomata are frequent in the liver in the course of 
the generalization of leukemic lymphadenoma ; but it has not as yet 



554 



TEXT-BOOK OF PATHOLOGY. 



been fully determined to what extent these are to be considered 
as true tumors, and to what extent as mere infiltrations of leuko- 
cytes consequent upon the enormous leukocytosis of this disease. 
Similar lyniphomatous nodules, though much less marked and 
numerous, occur in typhoid fever and other infectious diseases. 

Adenoma of the liver is met with in several forms. There 
may be either nodular masses, more or less encapsulated and of 
grayish-white or pinkish color, or a form of dhTuse infiltration of 
the liver-substance by encapsulated nodules of similar character. 
Considerable cirrhosis of the liver may be associated with the 
latter cases, and they cannot be clearly distinguished from cir- 
rhotic cancer (see below). 

Carcinoma of the liver is rather rare as a primary tumor, but, 
like adenoma, may be nodular or diffuse. The nodular or massive 
cancer appears as a single mass of varying size, ofttimes sur- 
rounded by local metastatic nodules. On section the color is 
grayish or pinkish, and there may be central necrosis and soften- 




Fig. 257.— Cirrhotic cancer of the liver (Hanot and Gilbert). 



ing. Diffuse hepatic cancer occurs as a widespread and more or 
less uniformly distributed infiltrating growth. Not rarely in such 
cases there is associated cirrhosis, and the macroscopic appearance 
of the liver may be strikingly like that of an ordinary cirrhosis, 
though the liver is sometimes much enlarged (Fig. 257). The 
terms cirrhotic cancer and cancer with cirrhosis have been applied 
to this form. Finally, the diffuse form may surround and spring 



DISEASES OF THE G ASTRO-INTESTINAL TRACT 555 



from the periportal structures, and may ramify in the form of an 
interlobular infiltration. 

Formation and Structure of Adenomata and Carcinomata. — ■ 

Microscopically there is no sharp dividing-line between these 
growths. The adenomata present tubular formations of a more or 
less elongated and tortuous character, composed of cylindrical or 
of more irregular-shaped epithelial cells. In some instances these 
are strikingly like new-formed biliary capillaries, and perhaps 
they occasionally originate from these structures. More com- 
monly, however, the origin would seem to be from the hepatic 
cells themselves. The columns of hepatic cells undergo prolifera- 
tive change, and at the same time become somewhat transformed, 
assuming the tubular arrangement of adenoma. Occasion- 
ally adenoma and cystic adenoma originate from the mucous 
glands of the larger biliary ducts. When cirrhosis is associated 
with adenomatous infiltration it is probable that the primary 
change is a cirrhotic overgrowth which induces secondary hyper- 
plasia of the epithelial cells, instead of degenerative changes, such 
as usually result from the pressure of new-formed fibrous tissue. 

Carcinoma of the liver is similar in origin and structure to 
adenoma. The cellular acini and tubules are more irregular, and 
there is an evident tendency to diffuse infiltration and atypical 
formation of acini. 

Secondary carcinoma of the liver is very common as a 
result of carcinoma of the stomach or of other parts of the portal 




Fig. 258.— Metastatic nodules of carcinoma on the surface of the liver (Hanot and Gilbert). 

distribution. It is usually due to cancerous embolism in the por- 
tal capillaries, with subsequent development of the emboli (Fig. 
259). The liver becomes enlarged, and presents nodular masses 
upon its surface or within its substance. These nodules vary 
from the size of a pea to that of an apple, and are frequently 



556 



TEXT-BOOK OF PATHOLOGY. 



sharply delimited by capsule-formation, especially those which 
have reached considerable size. Not rarely the nodules are in- 
dented upon the surface (umbilicated) from central softening or 
from contraction of fibrous tissue within (Fig. 258). Secondary 
cancer of the liver may also result from direct extension of cancer 
of the stomach or of the gall-bladder and biliary ducts. In all 
cases the new growths tend to compress the bile-ducts and lead 
to biliary pigmentation of the liver-substance, as well as to gen- 
eral icterus. 



Fig. 259.— Secondary cancer of the liver : a, columns of liver-cells filled with bile-pig- 
ment; b, endothelial walls of capillaries; c, carcinomatous emboli in the capillaries 
(Hanot and Gilbert). 

Cysts of the liver are rare. They may spring from the biliary 
ducts which have suffered simple dilatation, or from the mucous 
glands of the larger bile-ducts (cystic adenoma). Occasionally 
small cysts are seen which suggest origin from dilatation of the 
lymphatic channels. 

PARASITES. 

Of the protozoa, coccidial Psorospermice (Fig. 260) have been 
occasionally demonstrated in the human liver in small nodular 
tumors ; but a more important parasite is the Amoeba coli, occur- 
ring in abscess of the liver secondary to amebic dysentery. The 
pus of the abscess may contain immense numbers of the amebae, 
and doubtless these organisms bear an important relation to the 
lesion, perhaps causing necrosis by their own activity and then 



DISEASES OF THE GASTR O-INTESTINA L TRACT. 557 

liberating pyogenic organisms which they have carried from the 
intestines, and which complete the pathologic process. The larval 
Pentastoma denticulatum is occasionally met with. 

The Distoma hepaticum and the Distoma lanceolatum occasion- 
ally infest the biliary ducts, and the Distoma hematobium the portal 
vein. Ascarides sometimes creep upward in the biliary ducts as 
far as the branches within the liver. The Cysticercus cettulosce is 
a rare parasitic formation. 

Echinococcus cyst, — The most important parasitic disease of 




Fig. 260.— Coccidia in the wall of a bile-duct and the adjacent hepatic structure of a 

rabbit. 

the liver is the echinococcus-cyst, caused by the presence of the 
larvae of the Taenia echinococcus (see Part L). This parasite 
occasions cystic formations of various kinds within the liver. The 
cyst has a double wall : the outer, of connective tissue ; the inner, 




Fig. 261.— Echinococcus multilocularis (Luschka). 

a parenchymatous membrane, from which buds (brood-capsules) 
and secondary cysts are prone to originate. There may be a 
single cyst containing clear liquid of low specific gravity, or a 
mother-cyst containing daughter-cysts, either upon the inner wall 



558 



TEXT-BOOK OF PATHOLOGY. 



or floating free within the liquid after their separation. Some- 
times even granddaughter-cysts are formed. Occasionally the 
daughter-cysts are found outside of the mother-cyst, extrusion in 
such cases having taken place. A form of multilocular cyst is 
more rarely observed in which there are numerous small cysts 
embedded in more or less firm connective tissue (Fig. 261). 
Echinococcus-cysts may rupture into the abdomen or into sur- 
rounding viscera. The most serious condition is rupture into the 




Fig. 262.— Echinococcus-cyst of the liver (from a specimen in the Museum of the Phila- 
delphia Hospital). 

vena cava, as the result of which hydatid disease of the heart, the 
brain, or other organs may ensue. Bacterial invasion occasionally 
takes place, and abscess may result. Finally, the liquid contents 
may be absorbed, and the cyst may be reduced to a small cavity 
having a shrivelled wall and containing granular or caseous 
detritus (Fig. 262). Echinococcus-cysts may press upon the gall- 
duct, producing jaundice, or upon the portal veins, causing ascites. 

THE BILIARY DUCTS AND GALL-BLADDER. 
INFLAMMATIONS. 

Cholangitis, or inflammation of the biliary ducts, is 

most frequently secondary to duodenal catarrh, though it may be 
the result of direct irritation by gall-stones, by foreign bodies 
which have entered from the intestine, or by parasites or bacteria. 
In the cases secondary to duodenitis the inflammation usually 
extends but a short distance upward from the mouth of the com- 
mon bile-duct, but there may sometimes be more extensive in- 
volvement of the ducts, and the mucous membrane of the gall- 
bladder may be affected at the same time. The mucosa is swollen, 
more or less edematous, and secretes abundant mucus. The 



DISEASES OF THE GAS TR O-INTES TINA L TRACT. 559 



result is obstruction of the duct with retention of bile and jaun- 
dice. 

Suppurative cholangitis may result from bacterial in- 
vasion and fermentation of retained bile, or, in a localized form, 
from the impaction of a gall-stone. More rarely it is due to 
rupture of suppurative foci in the liver into the gall -ducts ; and 
occasionally it has been found as an independent affection asso- 
ciated with pyemia or other infectious diseases. Among the 
micro-organisms discovered in suppurative cholangitis the pyo- 
genic micrococci and the Bacillus coli communis are most fre- 
quent. The bile-ducts are filled with more or less decomposed 
bile, or with puriform liquid, and the walls of the ducts, espe- 
cially the larger ones, may present an ulcerated or necrotic ap- 
pearance. Small dilatations may occur in places where the duct 
has become deeply ulcerated, and later hepatic abscesses of con- 
siderable size may form. 

Chronic cholangitis may be the outcome of an intense 
acute or repeated acute attacks, but is more commonly met with 
as a consequence of chronic obstruction of the ducts and retention 
of bile. A localized form, causing cicatricial stenosis, results from 
intense inflammatory lesions following the passage of stones. The 
gall-ducts in chronic cholangitis are more or less thickened, and 
in the cases due to obstruction may be considerably dilated. 

Results of Cholangitis. — In the acute form extension may take 
place to the ducts within the liver, and in case of bacterial in- 
vasion pericholangitis and abscesses may form. More commonly 
acute cholangitis leads to but a temporary overfilling of the biliary 
capillaries with bile, and in consequence to obstructive jaundice. 
When the obstruction is continued for a considerable length of 
time reactive changes occur in the liver, constituting the form of 
cirrhosis called biliary cirrhosis (see page 550). 

Cholecystitis, or inflammation of the gall-bladder, 
may result from extension of cholangitis, or may be due to the 
irritation of retained bile or of gall-stones. It is a fairly common 
sequel of typhoid fever, and the typhoid bacillus has been found 
in the contents of the gall-bladder, sometimes a considerable time 
after the original infection had subsided. It is prone to assume 
a purulent character; and the gall-bladder may become filled 
with pus {empyema of the gall-bladder). This may rupture, dis- 
charging into the abdominal cavity, into adjacent viscera, or ex- 
ternally. The wall of the gall-bladder is usually much thickened, 
and the mucous membrane is swollen and ulcerated. 

STENOSIS AND DILATATION. 

Stenosis of the bile-ducts is most commonly the result of 
acute inflammation, causing thickening of the mucosa and ac- 
cumulation of mucus. It may result from chronic cholangitis 



560 



TEXT-BOOK OF PATHOLOGY. 



with cicatricial overgrowth of connective tissue ; from the impac- 
tion of gall-stones, or the presence of various foreign bodies, such 
as particles of food, mucus, round-worms or other parasites within 
the duct ; from pressure by aneurysms, by tumors of the head of 
the pancreas, pylorus, duodenum, lymphatic glands, or of the 
liver ; and from tumors of the gall-ducts themselves. Sometimes 
it is due to the constriction of adhesions resulting from peritonitis. 
Obstruction of the ducts leads to the retention of bile and dilata- 
tion of the ducts above, with consequent enlargement of the liver 
and jaundice. Obstruction of the cystic duct, which is most fre- 
quently due to the impaction of a stone, may occasion dilatation 
of the gall-bladder with dropsical liquid, in consequence of the 
passive hyperemia produced by compression of the veins at the 
neck of the gall-bladder. This condition is spoken of as dropsy 
of the gall-bladder. Sometimes suppurative inflammation occurs, 
and empyema of the gall-bladder results. 

Contraction of the gall-bladder, or even complete shrink- 
age or atrophy, may result from obstruction at the mouth of the 
cystic duct, or from inflammatory processes within its walls or 
surrounding it. 

Dilatation of the ducts or of the gall-bladder most frequently 
results from stenosis of the ducts below. 

GALL=STONES ; CHOLELITHIASIS. 

Gall-stones are concretions resulting from inspissation of bile, 
or from the deposit of various substances from the bile. Most 
frequently they are formed in the gall-bladder ; occasionally they 
originate in the bile-ducts. 

Etiology. — The causes are imperfectly understood. Ad- 
vanced years, the female sex, sedentary life, and high living seem 
to be factors of importance. Inflammatory conditions leading to 
obstruction and retardation of the outflow of bile, and also to des- 
quamation of epithelium, which, with mucus, serves to form the 
nuclei of the stones, seem to be among the causes. Besides these 
conditions there are probably indefinite alterations of the bile 
which permit of precipitation of some of its constituents, notably 
cholesterin. Bacterial decomposition of the bile and inflammation 
of the ducts, causing epithelial desquamation, are regarded as im- 
portant factors by some authorities. 

Structure and Pathologic Anatomy. — Gall-stones may 
be single or multiple, and may vary in size from minute granular 
particles of biliary sand to calculi several centimeters in diameter. 
When single they occur as rounded or oval masses ; when multiple 
they are prone to be marked with facets ; when formed within the 
bile-ducts they are elongated. Biliary sand is, for the most part, 
composed of biliary pigments in combination with calcium salts. 
The larger stones on section usually show a central nucleus com- 
posed of epithelium or mucus mingled with inspissated bile, sur- 



DISEASES OF THE GASTR 0-INTEST1NAL TRACT. 561 



rounded by a zone of somewhat radiating and crystalline structure, 
composed of cholesterin. Around this may be a coat of bile-pig- 
ment. In other cases the entire stone is formed of biliary pig- 
ments in combination with calcium salts, or more rarely the 
calculus consists entirely of carbonate of lime. 

Gall-stones may lie in the gall-bladder or ducts without caus- 
ing serious disturbances, or from time to time attacks of biliary 
colic denote their passage through the ducts to the bowel. They 
may pass through the ducts into the intestine w T hen of small size, 
but often become impacted in the lower part of the common duct, 
generally just above the duodenal papillae or in the mouth of the 
cystic duct. Secondary changes in the gall-bladder (dilatation and 
inflammation) and in the liver (enlargement, cirrhosis) may result ; 
and the stone may cause local ulceration, and may Anally escape 
into the bowel or into other parts by ulceration. Occasionally 
gall-stones remain impacted for long periods without causing 
serious disturbances, enough space remaining to permit the es- 
cape of bile. 

TUMORS. 

Tumors of the gall-ducts and gall-bladder are rare. Primary 
carcinoma arising from the mucous glands is the most important. 
This appears as an irregular elevation of the mucous surface, and 
rapidly infiltrates the adjoining parts. In cases of primary cancer 
of the gall-bladder the liver is soon involved. Gall-stones are 
present in a great majority of the cases and probably play an im- 
portant etiologic part by their continuous irritation. On the other 
hand, the gall-stones may form in consequence of the stagnation of 
bile and other local conditions caused by the tumor. Secondary 
carcinoma of the gall-bladder or ducts most frequently results 
from cancer of the liver. The lower end of the duct may be in- 
volved in cases of carcinoma of the papilla of Vater. Sarcoma, 
fibroma, and other tumors are rare. 

e 

JAUNDICE. 

Jaundice, or icterus, is a discoloration of the skin and other 
parts, resulting from the presence in the blood of biliary pigments. 

Etiology. — Jaundice has been described as being of two forms, 
the obstructive, mechanical, or hepatogenous, and the non- obstructive 
or hematogenous variety. This distinction, hoAvever, has been to 
a large extent abandoned, and it is now admitted that the abnor- 
mal coloring-matter in all cases originates in the liver, and is in- 
variably a hepatic pigment. 

Among the distinctly mechanical causes of jaundice the most 
frequent is occlusion of the ducts by catarrhal duodenitis and 
cholangitis. To this form the term catarrhal jaundice is generally 
applied. Less commonly obstruction may be occasioned by for- 
eign bodies, gall-stones, or parasites within the ducts ; by the 

36 



562 



TEXT-BOOK OF PATHOLOGY. 



pressure of tumors of the duodenum, pancreas, and the lymphatic 
glands of the liver or of the gall-ducts themselves ; by the press- 
ure of aneurysms upon the ducts ; or by occlusion of the biliary 
passages within the liver by abscess, hydatid cysts, hypertrophic 
cirrhosis, carcinoma, or other tumors. Congestion of the liver 
may lead to jaundice by the swelling of the organ consequent upon 
the overfilling of the vessels with blood, or by reason of the re- 
sorption of bile due to the alterations of pressure of the blood in 
the different vascular channels. Hematogenous jaundice was for- 
merly regarded as due to disintegration of the blood in the gen- 
eral circulation, but it is now recognized that formation of the pig- 
ments can take place only in the liver. There are, however, in- 
stances of jaundice in which active hemolysis is an element of 
importance. Jaundice of this character occurs in various severe 
infections, such as yellow fever, acute yellow atrophy of the liver, 
the jaundice of the new-born, and in consequence of certain in- 
toxications (phosphorus, toadstools, the venom of snakes). Several 
explanations may be applied to cases of this kind. Sometimes 
excessive blood-destruction leads to formation of abnormally large 
quantities of bile (polycholia), and in consequence to absorption 
of biliary pigment by the lymphatics in the liver. It is believed 
by some investigators that the hepatic cells may in some condi- 
tions reverse the direction of their secretion, so that the bile is 
discharged into the lymphatic current instead of into the biliary 
capillaries. This view needs confirmation. In other cases toxic 
degeneration of the hepatic ceils may lead to stimulation of the 
hepatic function, or to swelling of the cells and compression of the 
biliary capillaries, and in consequence to absorption of the bile. 
Finally, in the jaundice of the new-born, as well as in some 
instances of sudden emotional jaundice, disturbance of the circula- 
tion within the liver may be a potent cause. 

Pathologic Anatomy. — Microscopic examination of the liver 
may show the biliary capillaries distended with bile and the 
hepatic cells themselves more or less pigmented. The bile is 
absorbed by the lymphatics, and ultimately reaches the general 
circulation and pigments the tissues. The earliest evidence is 
seen in the intima of the vessels ; later, all the tissues and organs 
of the body may be involved, and visible discoloration appears in 
the skin and external mucous membranes. The urine is dark 
brownish or greenish in color, and all of the secretions and liquid 
exudates may be pigmented. In cases caused by obstruction of 
the bile-ducts the bile cannot reach the intestines and the stools 
have a quite characteristic putty color. In " hematogenous " 
jaundice the color of the stools is to a certain extent maintained. 
Intense disturbances, especially of the nervous system, result from 
excessive cholemia, but are due to the cholic acid salts, rather than 
to the biliary pigments. 



DISEASES OE THE G ASTRO-INTESTINAL TRACT 563 



THE PANCREAS. 

CONGENITAL ABNORMALITIES. 

Complete absence has been met with in monstrosities. More 
frequently an adventitious pancreas or heterotopic pancreatic 
tissue is observed. Small nodules of pancreatic tissue may be 
found in the omentum, the wall of the intestines, or elsewhere. 

CIRCULATORY DISTURBANCES. 

Active hyperemia occurs during digestion and in association 
with acute inflammation. 

Passive hyperemia occurs in cases of obstruction to the 
portal circulation, but rarely leads to notable changes. 

Hemorrhage may occur in the pancreas, in the form of 
minute petechia? or diffuse hemorrhagic infiltration, as the result 
of passive congestion or of various hemorrhagic and infectious 
diseases, such as purpura, scurvy, septicemia, or the extreme 
anemias. 

More extensive hemorrhage in the pancreas and in the tissues 
surrounding it sometimes occurs as an " idiopathic " affection, the 
causes being obscure. It is more common in the young than the 
old, and in the male than the female sex, and at times appears to 
be dependent upon traumatism. Doubtless in some cases the hem- 
orrhage is the result of necrosis or other pre-existing affections of 
the pancreas or of its blood-vessels. The changes are most marked 
in the head of the organ, although any part may be affected. There 
may be diffuse infiltration, or the hemorrhage occurs in isolated 
foci. Occasionally considerable collections of blood may be met 
with, and secondary reactive inflammation and necrosis are fre- 
quently observed. The peritoneum, the wall of the duodenum, 
and other surrounding tissues may be coincidently involved. 

Sudden death may occur in this condition from shock or com- 
pression of the solar plexus, or the case may terminate in other 
pancreatic affections. Doubtless chronic indurative pancreatitis 
originates in this way in some cases. More commonly progressive 
necrosis and suppurative inflammation terminate the disease. 

ATROPHY AND DEGENERATIONS. 

Atrophy of the pancreas occurs in old age and as the 

result of marasmic conditions. The entire organ is involved in 
such cases. Localized atrophy may be associated with various 
degenerations or other diseases of the organ. Thus, in carcinoma 
or in cirrhosis pressure-atrophies are extremely frequent. 

The association of atrophy of the pancreas with diabetes is a 
most important one, and it may be assumed that certain cases of 
diabetes are Avholly dependent upon disease or atrophy of this 



564 



TEXT-BOOK OF PATHOLOGY. 



organ. Though atrophy is the most common pancreatic condition 
in diabetes, cirrhosis, carcinoma, and calculous obstruction of the 
ducts have been observed. It is believed by some that the pan- 
creas elaborates sugar-destroying ferments whose presence in the 
blood is necessary to prevent hyperglycemia. In diseases of the 
pancreas this ferment is lacking and glycosuria results. 

Parenchymatous degeneration may occur in consequence 
of acute infections, and resembles the cloudy swelling of the liver, 
kidneys, and heart occurring in the same diseases. The organ 
becomes somewhat enlarged ; is softer than normal ; and may at 
the same time be congested. 

Microscopically the cells are found to have undergone granular 
degeneration. 

Amyloid degeneration is a rare condition occurring in 
association with amyloid disease of other organs. 

Pigmentation may be met with in the atrophic organ of old 
persons, or in consequence of hemorrhagic infiltration and subse- 
quent disorganization of the extra vasated blood. Of particular 
interest are the cases of hematochromatosis affecting the pancreas, 
together with the intestines, liver, and other abdominal organs in 
drunkards. The affected organs in this condition present more or 
less extensive hematogenous pigmentation. 

Necrosis of small areas of the pancreas may occur in conse- 
quence of hemorrhage or of inflammatory conditions. Sometimes 
the entire organ is disorganized by a form of gangrenous necrosis, 
especially in case of pancreatitis resulting from perforation of a 
gastric ulcer or from extension of other severe inflammatory 
lesions. 

Fat-necrosis is a form of degeneration or necrosis peculiar 
to the fatty tissue of the pancreas and of the omentum. Most 
frequently it is found in association with acute or chronic pancrea- 
titis, with tumors of the pancreas, or obstruction of its duct ; but 
it may occur independently, and it may appear in the fatty tissue 
of the omentum without involving the pancreas. Minute foci, 
having a gray or white, opaque appearance, or more rarely larger 
areas due to confluence of small foci of necrosis, are found 
in the adipose tissues. Hemorrhagic infiltration may be asso- 
ciated, and sometimes extensive hemorrhage may ensue. Inflam- 
mation of the pancreatic tissues around the foci of necrosis is com- 
mon, and in some instances extensive disorganization (necrosis) of 
the pancreas occurs. 

Microscopically the changes consist of, first, the formation of 
fat-crystals within the adipose cells, and subsequently the dis- 
organization of these and the formation of calcium salts of the fat- 
acids, the microscopic appearance at this stage being that of indefi- 
nite granular or translucent masses. The nature of fat-necrosis 
has been previously discussed (see page 97). 



DISEASES OF THE GA STB O-INTESTINA L TRACT. 565 



INFLAMMATIONS, 

Pancreatitis may be acute or chronic. The acute variety 
presents itself in different forms, the most frequent being the 
hemorrhagic and the suppurative or necrotic. Chronic pancrea- 
titis is analogous to chronic hepatitis, and leads to similar indura- 
tion or cirrhosis. 

Acute hemorrhagic pancreatitis occurs most commonly in young 
persons, and is probably in most, if not all, cases dependent upon 
infection of the pancreas through its ducts. It is likely that some 
cases are not in reality inflammatory, but simply instances of 
degenerations of the pancreas, with hemorrhage and round-cell 
infiltration as consequences. The pancreas is swollen, especially 
at its head ; the lobules are enlarged and the interlobular tissues 
compressed. Hemorrhagic infiltration is a constant condition, but 
variable in extent. Microscopically the cells of the pancreas are 
swollen, and usually present the appearances of parenchymatous 
degeneration. The interlobular tissues are infiltrated with round 
cells. Localized necrosis and fat-necrosis may be associated. 
Rapid death is the usual consequence, but it is probable that 
some of the cases terminate in chronic pancreatitis. 

Acute suppurative or necrotic pancreatitis may result from 
direct extension of septic processes in the neighborhood, as in gas- 
tric or duodenal ulceration, purulent collections in the peritoneum, 
and the like. It may also occur as an independent affection, most 
frequently in consequence of infection from the intestinal tract 
through the ducts. Occasionally metastatic abscesses are observed 
in the pancreas. Hemorrhagic pancreatitis may be converted into 
the necrotic form in consequence of extensive extravasation of 
blood and secondary infection. 

The organ presents a variable appearance, according to the 
cause and extent of the process. There is generally marked 
swelling with more or less softening, and not rarely necrotic foci. 
Complete gangrene or necrosis is an occasional termination. In 
other cases parts of the pancreas may slough, and may be dis- 
charged through the intestines or into the peritoneum, setting up 
fatal peritonitis. 

Chronic indurative pancreatitis, or cirrhosis of the pancreas, may 
be hematogenous in origin, resulting from syphilis and alcoholism, 
or it may be caused by prolonged irritation exercised through the 
pancreatic ducts. In the latter case it may be secondary to duod- 
enal catarrhs or obstructions of the pancreatic duct. In some 
cases it is doubtless the outcome of acute attacks. 

The pancreas in the earlier stages is enlarged and hard. On 
section it may present a homogeneous structure and may be of 
cartilaginous consistence. Macroscopically the tissues between 
the acini are visibly infiltrated and hyperplastic, the amount 



566 



TEXT-BOOK OF PATHOLOGY. 



of connective tissue being greatly in excess of the normal. In the 
later stages the organ becomes contracted, and may be consider- 
ably reduced in size and of stony hardness. 

Microscopically the parenchyma of the organ is found to be 
atrophied or degenerated in consequence of contraction of the 
hyperplastic fibrous tissue. Fat-necrosis and fatty degeneration 
of the pancreatic cells are frequently associated. 

INFECTIOUS DISEASES. 

Syphilis may occur in the pancreas in the form of indurative 
pancreatitis or of gummata. The former may occur in adults, but 
is more common in the new-born, in association with indurative 
changes in the liver, lungs, and other organs. 

Tuberculosis of the pancreas, in the form of miliary 
tubercles, may occur in cases of generalized tuberculosis. 

TUMORS. 

Primary benign tumors have occasionally been met with, but 
are unimportant. 

Carcinoma. — Primary cancer may affect the head or other 
parts of the pancreas, and is of the glandular (scirrhous), or, more 
rarely, of the cylindrical-celled, variety. Compression with sec- 
ondary cystic distention of the pancreatic duct and obstruction of 
the common bile-duct or of the veins (portal, superior mesenteric, 
and splenic) behind the head of the organ may result. Metastasis 
to the neighboring lymphatic glands and to the liver is frequent. 
Secondary cancer may affect the pancreas by extension of cancer 
of the stomach or of the duodenum. 

Pathologic Physiology. — Pancreatic carcinoma, and other chronic 
diseases of the pancreas, often occasion rapid emaciation, and some- 
times fatty diarrhea, lipemia, and lipuria. Reference has already 
been made to the occurrence of diabetes (glycosuria) in pancreatic 
diseases. In a mechanical way cancer of the head of the pancreas 
may cause jaundice by obstruction of the bile-ducts ; splenic en- 
largement, intestinal congestion, diarrhea, and ascites by obstruc- 
tion of the adjacent veins ; repeated vomiting and sometimes 
intestinal obstruction by compression of the duodenum. 

Sarcoma is rarely primary. Secondary nodules are occasion- 
ally observed. 

Cysts of the pancreas may be of several kinds. Dilatation of 
the pancreatic duct or its branches may occasion a single cyst or 
multiple cysts filled with serous or gelatinous liquid. Hemorrhagic 
cysts are sometimes the result of necrosis of portions of the organ, 
or a primary hemorrhage (hematoma) may be converted into a 
serous cyst. The latter is the mode of formation of some of the 
large cysts occurring, for the most part, near the tail of the pan- 



DISEASES OF THE GAS TR O-INTES TINA L TRACT. 



567 



creas. In other cases, it has been held, these cysts result from 
primary necrosis and subsequent digestion of the necrotic area by 
the pancreatic secretions. In rare instances cysts of the pancreas 
have a glandular structure somewhat resembling that of ovarian 
cystomata. 

Cystic accumulations in the lesser omental cavity, resulting from 
localized peritonitis, may be difficult to distinguish from true pan- 
creatic cysts, as some of the latter lie more outside than within the 
pancreas. In some instances such localized peritonitis seems to 
be the result of extension of pancreatic inflammations. 

The fluid of pancreatic cysts often contains a proteolytic and 
an emulsifying ferment, but the contents of other abdominal cysts 
may have similar constituents. 

The Pancreatic Duct. 

Obstruction of the pancreatic duct may be due to tumors of 
the papilla in the duodenum or of the head of the pancreas, to 
calculi, to inflammatory thickening of the duct itself, or to the 
pressure of contracting fibrous tissue in chronic pancreatitis. 
Most commonly it leads to dilatation of the duct, this sometimes 
becoming so great as to occasion actual cystic formations (Fig. 
263). The dilated ducts are filled with clear liquid, but some- 




Fig. 263.— Dilatation of the pancreatic duct and atrophy of the pancreas, due to calculi 

(Orth). 

times through bacterial infection this is rendered turbid, or is 
actually converted into pus. Occasionally small cysts, caused 
by distention of the finer divisions of the duct, are scattered 
through the organ (pancreatic acne). These are supposed to 
result from catarrhal processes in the ducts themselves. These 
small cysts are filled with clear or puriform liquid. Some cases 
so described are doubtless instances of fat-necrosis. 

Pancreatic calculi are composed of carbonate or phosphate 
of lime, and usually have an irregular shape. They may occasion 
cystic distention of the ducts and abscess-formation. 



568 



TEXT-BOOK OF PATHOLOGY. 



THE PERITONEUM. 

CONGENITAL ABNORMALITIES. 

Absence of the peritoneum has been described; but more 
frequently minor defects, such as absence of the omentum or 
unnatural length of the omentum or mesentery, localized defects, 
fenestrations, and the like, have been observed. The peritoneal 
extension into the inguinal canal normally becomes occluded, but 
may remain patulous and may lead to congenital hernia. 

CIRCULATORY DISTURBANCES. 

Active hyperemia may occur in association with inflam- 
mation, or in the vicinity of lesions within the intestine which 
have not yet occasioned actual inflammation of the peritoneum 
itself. The affected part is bright red, the arterioles being dis- 
tended and the endothelium somewhat swollen and elevated. 

Passive hyperemia is more frequent. It may be part of a 
general venous congestion, or may result from obstruction of the 
portal vein by thrombosis, cirrhosis of the liver, and similar con- 
ditions. The venules may be widely dilated, the deeper layers of 
the peritoneum somewhat edematous, and the lining endothelium 
swollen and loosened. Intense passive congestion may lead to 
ascites or to hemorrhage. 

Hemorrhage may occur in the form of punctate extravasa- 
tions in various septic and hemorrhagic diseases, and in parts 
adjacent to intense inflammatory lesions, as in the peritoneum 
covering the bowel near anthrax-ulcerations. Hemorrhagic 
extravasations may likewise be due to intense passive congestion, 
as in death from suffocation or in obstructions of the portal circu- 
lation. Certain forms of intoxication, like phosphorus-poisoning, 
snake-venom, or the like, may occasion petechial ecchymosis or 
large suffusions ; and occasionally hemorrhagic extravasations are 
due to embolic occlusion of the mesenteric arteries. Large 
hemorrhagic effusions may occur in the retroperitoneal tissues, 
especially at the root of the mesentery, between the folds of the 
omentum, or elsewhere into the subperitoneal cellular tissues. 
These, as well as hemorrhages into the peritoneal cavity itself, are 
frequently traumatic in origin. Rupture of the spleen, of the 
liver, of the uterus or Fallopian tubes, or of aneurysms or 
superficial blood-vessels may be the immediate source of large 
hemorrhages. 

The extravasated blood within the cellular tissues undergoes 
gradual absorption, as elsewhere, and may leave pigmented areas 
and fibrous thickening. The blood within the cavity of the peri- 
toneum may be directly absorbed, or may be gradually removed 



DISEASES OF THE GASTR O-IXTESTIXAL TRACT. 569 



after clotting by degenerative processes and absorption through the 
lymphatic channels. Inflammatory reaction is wanting unless the 
blood-mass is infected. 

Dropsy of the peritoneum, or ascites, may occur as a 
part of a general anasarca in cardiac or renal disease, or may be 
due to obstruction of the portal circulation, notably by cirrhosis 
of the liver. In these cases ascites may be absent at first from 
the freedom of the collateral circulation established between the 
branches of the inferior and superior vena cava and the peripheral 
radicles of the portal circulation. Eventually, however, ascites 
ensues. In the earliest stages of certain cases of intense acute 
peritonitis and in chronic peritonitis, especially the tuberculous 
form, when the absorption of liquid from the peritoneum is dis- 
turbed by occlusion of the lymphatics, the liquid effusion may have 
a serous and not the ordinary inflammatory character. Chronic 
peritonitis plays a part in the etiology of many cases of ascites 
ordinarily regarded as the result of obstruction of the circulation 
alone, as in cases of cirrhosis of the liyer. In such cases the 
venous stasis may occasion no dropsical exudation until a low- 
grade chronic peritonitis has developed, when the membrane 
becomes more permeable and effusion results. 

An occasional cause of ascites is obstruction of the thoracic 
duct by new-growths of its walls, thrombosis within, or pressure 
from the outside. The ascitic liquid in such cases frequently has 
a chylous character. 

The abdomen in ascites is filled with clear watery or yellowish 
liquid. Gelatinous masses often form in the dependent parts, as 
in the pelvis and iliac fossae. Occasionally the liquid is quite 
hemorrhagic ; in other cases it is milky from admixture of chyle 
or lymph (chylous ascites). The latter cases are dependent upon 
obstruction and rupture of the lymphatic channels. In other 
cases, especially in instances of endothelioma or carcinoma of the 
peritoneum, the liquid has a milky character from admixture of 
degenerated cells and fatty matter. The term chyliform ascites is 
sometimes applied to such cases. Microscopically the liquid of 
ordinary ascites shows red and white blood-corpuscles and occa- 
sionally a few endothelial cells. In the hemorrhagic cases the 
number of blood-corpuscles is notably increased, while in chylous 
ascites there are fat-droplets and granular cells. 

Occasionally collections of dropsical liquid occur between the 
layers of the omentum (hydrops oment'i). 

Ascites causes more or less serious compression and displace- 
ment of the abdominal organs. The respirations may be greatly 
embarrassed by upward displacement of the diaphragm, and the 
circulation may be obstructed by the pressure of the liquid upon 
the veins. Secondary changes in the peritoneum are not unusual. 
Long-standing ascites nearly always gives rise to a certain amount 



570 



TEXT-BOOK OF PATHOLOGY. 



of chronic inflammation (fibrous thickening of the membrane), and 
termination in tuberculous peritonitis is not infrequent. 

INFLAMMATIONS. 

Inflammation of the peritoneum, or peritonitis, is the 

most important condition of this structure. Acute and chronic 
cases may be distinguished. The latter, in most instances, merely 
represent terminal conditions following acute forms of the disease. 
Exceptionally, peritonitis may be a chronic alfection from the 
beginning. 

Etiology. — Acute peritonitis is probably always caused by 
bacteria or bacterial products. It is possible to produce it in 
animals by injections of chemical poisons into the peritoneum, but 
it is doubtful if spontaneous peritonitis ever occurs, excepting as 
a result of infection. 

The bacteria gain access to the peritoneum through the blood, 
by direct migration from the Fallopian tubes, by invasion through 
the walls of the abdominal viscera, or by perforation of the viscera 
or external abdominal Avails. Hematogenic peritonitis is some- 
times met with in cases of general septicemia and pyemia, as in 
osteomyelitis or malignant endocarditis, but such cases are rare. 
In these instances the bacteria may be discharged into the peri- 
toneal cavity from the blood, and may thus occasion a direct or 
primary peritonitis ; more frequently a localized lesion, such as a 
suppurating infarction, is first produced and the peritonitis results 
secondarily from this. Undoubtedly bacteria are often set free in 
the peritoneum in the course of infections, but this structure seems 
to have a high degree of resistance, and seems to be possessed of 
special means of defence. The experiments of Pfeiffer with re- 
gard to the mechanism of immunity (see page 205) may be cited 
in this connection. Idiopathic peritonitis was a term used by 
older authors to designate forms of seemingly causeless peritonitis, 
or such as follow exposure to cold and the like. At the present 
time we must regard these as exceptional instances of primary 
hematogenic peritonitis, or more commonly as cases of secondary 
peritonitis resulting from abdominal infections that have been 
overlooked. 

Peritonitis resulting from direct extension of infective pro- 
cesses is very common. A certain amount of irritation of the 
serous coat (the peritoneum) of the abdominal organs occurs in 
most of the diseases of these organs, and in the case of certain 
infectious diseases this may attain considerable intensity. For 
example, in cases of ulcers of the intestines or strangulation of 
a coil of intestine with secondary necrosis, considerable peritonitis, 
local and eventually general, may occur without perforation of the 
gut. In such cases the bacteria penetrate the walls of the intes- 



DISEASES OF THE GA S TR O-INTESTINAL TRACT. 571 



tines along the lymphatic channels, and thus reach the serous 
covering. Similar extensions are found in diseases of the tubes 
and ovaries, or of the uterus in puerperal sepsis. 

Perforative peritonitis is the most important of the forms. It 
may result from perforation of gastric ulcers or cancer, from trau- 
matic or ulcerative perforations of other parts of the intestinal 
tract, from perforation of the appendix in acute appendicitis, or 
from rupture of diseased Fallopian tubes ; less commonly perfora- 
tion of the other abdominal viscera, or rupture of infective foci, 
such as abscesses of the spleen, liver, pancreas, ovaries, or other 
structures, or penetration of the abdomen from without by stab- 
wounds or disease, may lead to peritoneal infection. 

Among the micro-organisms that have been detected, the 
Streptococcus pyogenes is most important, and is the cause of the 
severest forms of peritonitis, such as those occurring in puerperal 
sepsis. Occasionally the disease is due to the Staphylococcus 
pyogenes, the Bacillus coli communis, the Diplococcus pneumoniae 
the bacillus of Fried-lander, the gonococcus, or other organisms. 
The Bacillus coli is mainly operative in peritonitis secondary to 
intestinal diseases, such as appendicitis. Very often, no doubt, 
peritonitis is the consequence of mixed infection. 

Pathologic Anatomy. — Localized and general peritonitis may be 
distinguished. 

Acute localized peritonitis is seen in cases in which 
bacteria escape gradually and in small numbers through the 
walls of the viscera, or in instances in which perforation takes 
place after the production of some exudate which serves the 
purpose of limiting the extension of the infection. Localized 
peritonitis is most frequent in the pelvis in association with 
diseases of the tubes or uterus, and in the region of the appen- 
dix. The peritoneum of the area of disease first becomes in- 
tensely injected (congested) and the normal luster disappears in 
consequence of the beginning exudation and disease of the lining 
endothelium. Subsequently the amount of exudate increases. It 
may, first, be of serous character, but usually is largely fibrinous, 
and the amount may be considerable. Thus the appendix is not 
rarely surrounded by masses of fibrinous exudate a centimeter or 
two in thickness. The exudate may remain fibrinous, but more 
frequently becomes fibrinopurulent in the later stages ; and in 
cases of perforative peritonitis localized abscesses are commonly 
met with. In such cases, if the disease remains well encapsulated, 
and the patient survives, the exudate may be removed in several 
ways. Very rarely the pus burrows toward the exterior and dis- 
charges ; more frequently it empties into the intestine or some 
other hollow viscus. It may decrease by gradual inspissation, 
leaving a dry, cheesy mass, which in rare instances finally be- 
comes calcareous. Fibrinous exudates in localized peritonitis 



572 



TEXT-BOOK OF PATHOLOGY. 



are frequently absorbed, and give place to fibrous-tissue adhe- 
sions. 

Acute general peritonitis may be the immediate result of the 
discharge of large quantities of infective matter from a perforated 
bowel or other organ ; or it may occur secondarily to a localized 
peritonitis when the limiting-wall of exudation is broken down. 
In these cases the peritoneal covering of the intestines, and to a less 
extent the parietal peritoneum, become congested and lusterless, 
as in the localized form. Serous exudation takes place, and may 
be considerable in amount in some of the most violent forms of 
the disease. Acute inflammatory ascites is thus produced. Usu- 
ally, however, the serous exudation is scanty, and very soon the 
intestines are covered with flakes or thin coatings of fibrinous 
exudate and are matted together. Subsequently the exudate 
grows more yellowish from the emigration of leukocytes or pus- 
cells. When adjacent coils of intestine are agglutinated by the 
exudate pockets containing serous or seropurulent liquid may be 
formed between them. 

In the most violent forms of peritonitis, local or general, such 
as those due to strangulation and gangrene of a part of the bowel, 
or to puerperal sepsis, the exudates may rapidly assume a putrid 
character, and the deposit upon the serous surface, as well as the 
serosa itself, may undergo necrotic change. In these cases the 
cavity of the peritoneum contains more or less ill-smelling brown- 
ish, grayish, or blood-tinged liquid exudate, and the affected areas 
of the peritoneum are covered with greenish or brownish deposits. 

Hemorrhagic peritonitis is sometimes observed. It represents 
no special form, but merely indicates systemic or local conditions, 
as a result of which hemorrhagic extravasation has taken place 
into the exudate. This is found in the peritonitis of scorbutic 
individuals or of persons reduced in vitality by other diseases. It 
also occurs when passive congestion is associated with peritonitis, 
as in cases of cirrhosis of the liver. The peritonitis accompany- 
ing tuberculosis, and especially carcinoma of the peritoneum, may 
present hemorrhagic exudate. 

Effects of Acute Peritonitis. — The disease of the peritoneum has 
an immediate and profound effect upon the intestines, and reflexly 
or in other ways upon the general system. The peristalsis of 
the bowel in the earlier stages is arrested by spasmodic contrac- 
tion. Very soon the musculature is paralyzed and more obstinate 
constipation results. The systemic effects are most strikingly 
evidenced by the intense shock of the early stages. General 
septicemia may be the consequence of the infective conditions of 
the peritoneum. 

Chronic peritonitis may be the termination of an acute 
peritonitis, especially the localized form. In other cases chronic 
inflammatory thickening occurs in the peritoneum adjacent to or 



I) TS EASES OF THE GASTR O-INTESTINAL TRACT. 573 



covering organs the seat of various diseases. Thus in cirrhosis of 
the liver the peritoneal covering and the reflexions forming the 
ligaments may be greatly thickened, and similarly the peritoneum 
covering the spleen may be involved in consequence of chronic 
congestion or inflammation of this organ. 

Chronic peritonitis following local acute peritonitis usually pre- 
sents itself in the form of fibrous thickenings or adhesions, such as 
are so often encountered in the pelvis after uterine, tubal, or ovarian 
disease complicated by peritonitis, and about the appendix after 
inflammations of this structure. Less commonly chronic perito- 
nitis is met with in the form of sacculated effusions. In such in- 
stances the effusion formed during the acute stage is only partially 
absorbed, and remains as an inspissated liquid. 

In other cases dense adhesions are formed, and occasionally cal- 
careous plates are found in the thickened peritoneal covering of the 
bowels or other parts. 

Chronic diffuse peritonitis may result from diffuse acute peri- 
tonitis. In such cases there are widespread adhesions, and the peri- 
toneum is more or less diffusely thickened. More or less liquid 
effusion may be present. In other instances diffuse peritonitis arises 
in an insidious manner as a chronic process from the beginning. 
Some of these cases are entirely obscure in etiology ; in a few it has 
seemed probable that syphilis was an etiologic factor. The perito- 
neum is often uniformly thickened, but in some cases presents small 
nodular lesions, suggesting miliary tubercles. In several instances 
these nodules, together with the abundant serous effusion occasion- 
ally met with, have led to the diagnosis of tuberculous peritonitis. 
Microscopic examination of the nodules, however, shows a fibrous 
structure, and neither giant-cells nor tubercle-bacilli. Tuberculous 
and malignant peritonitis will be considered below. 

Hyperplastic Perihepatitis. — A few cases have been observed of a re- 
markable disease in which the upper part of the parietal peritoneum and 
the reflexions covering the liver and spleen are greatly thickened and of 
dense sclerotic character. The peritoneum is sometimes several millimeters 
in thickness, gray or white, and suggests the appearance of the " icing " of 
confectioners. This has led to the term proposed by Curschmann — Zucker- 
gussleber. The liver and spleen undergo more or less pressure-atrophy, and 
ascites is a frequent symptom. The etiology is obscure. 

INFECTIOUS DISEASES. 

Tuberculosis may in rare instances affect the peritoneum 
primarily, as in cases in which tubercle-bacilli penetrate the 
mucosa of the intestines and enter the lymphatics without causing 
an intestinal lesion ; or in cases of infection through the Fallopian 
tubes. Usually tuberculosis of the peritoneum is secondary to 
tuberculosis of some abdominal viscus or of more distant organs. 
Thus among the more frequent causes are tuberculosis of the mes- 



574 



TEXT-BOOK OF PATHOLOGY. 



enteric or retroperitoneal glands and tuberculous disease of the 
tubes and ovaries in women. Intestinal tuberculosis rarely leads 
to more than localized lesions of the serous coat opposite the ulcera- 
tions of the mucosa. Pulmonary tuberculosis may occasion hema- 
togenic infection of the peritoneum. Simultaneous tuberculosis of 
various serous membranes, especially the pleura and peritoneum, 
is occasionally observed. The source of infection is often hidden ; 
sometimes the pleura is first involved and the peritoneum becomes 
affected by extension ; less commonly the reverse occurs. 

Pathologic Anatomy. — Miliary tuberculosis without marked in- 
flammatory changes may occur as a generalized peritoneal affection 
in acute or subacute general miliary tuberculosis. Local eruptions 
of similar character are seen in the pelvic peritoneum in cases of 
tubal or ovarian tuberculosis and upon the serosa of the intestines 
adjacent to tuberculous ulcers of the bowel. 

More important, from a clinical point of view, are the cases in 
which inflammatory changes are associated with the specific tuber- 
cle. In some instances extensive adhesions by fibrinous or fibrous 
productions are met with, while the tubercles tend to agglutinate, 
forming masses of considerable size and of cheesy character. The 
mesenteric lymph-glands may be coincidently involved, being en- 
larged and caseous. Sacculated collections of serous or seropuru- 
lent liquid are sometimes observed. In another variety there is 
abundant serous exudation. Occasionally the exudate is hemor- 
rhagic. 

Tuberculosis of the peritoneum sometimes terminates in com- 
plete resolution, the peritoneum being left somewhat thickened, 
but showing no other evidences of the previous disease. 

TUMORS. 

Fibromata and lipomata are sometimes met with as small 
nodular or pedunculated outgrowths from the subperitoneal tissues. 

Sarcoma may occur in the form of diffuse gelatinous tumors 
of angiosarcomatous structure, or in the form of endotheliomata. . 
The latter variety occasions diffuse thickening, sometimes of con- 
siderable areas, of the peritoneum. Secondary sarcoma is some- 
times observed as nodules of considerable size or as numerous mil- 
iary nodules. 

Carcinoma of the peritoneum is usually secondary. Gelati- 
nous or colloid cancers of the stomach and bowel (rectum) fre- 
quently extend widely through the peritoneum, causing great 
thickening and a remarkably gelatinous growth. Not rarely 
rounded masses of pearly appearance are observed (Fig. 74). In 
rare instances tumors of the peritoneum of the same general char- 
acter seem to be primary, and the reasonable explanation has been 
suggested that parts of intestinal tissue, pinched off in fetal de- 



DISEASES OF THE DUCTLESS GLANDS. 



575 



velopment, are the starting-points of the growths. Secondary 
cancer frequently appears in the form of nodular tumors in asso- 
ciation with ovarian cystomata that have become carcinomatous, 
or with primary cancers of the ovaries and other pelvic organs. 
Occasionally widespread eruption of miliary nodules is met with 
as a part of acute carcinomatosis. 

In all forms of carcinoma of the peritoneum inflammatory 
changes with intestinal agglutination and adhesion are frequent. 
Hemorrhagic exudation is not unusual. In rare cases the bowels 
are so firmly fused by the spreading tumor and the inflammatory 
exudates that they form a solid mass, which on section shows the 
cavities of adjacent coils of intestines separated by more or less 
uniform tumor-tissue. 

PARASITES. 

Bchinococcus-cysts occasionally occupy the peritoneal 
cavity, and may fill it almost completely. Filarial have been 
found in a few instances ; and the Pentastomum denticulatum and 
Cysticercus celluloses have been reported. Recently an ameboid 
organism (Leydenia gemmipara) has been discovered in the liquid 
exudate of cases of ascites. 



CHAPTER Y. 
DISEASES OF THE DUCTLESS GLANDS. 

THE THYROID GLAND. 

Anatomic Considerations. — The thyroid gland is a com- 
pound tubular gland, which in fetal life communicates with the 
pharynx at the base of the tongue by a duct. Later the duct is 
obliterated, and the gland becomes ductless. Microscopically 
there are found acini lined with polyhedral or cylindrical epi- 
thelium, usually in a single layer. The lumen of the acinus 
contains more or less gelatinous, or, as it is usually called, colloid 
material, which seems to be a secretion of the epithelium. It is 
an albuminate rich in sodium chloric!. The vascular supply of 
the gland is very abundant, the blood-vessels being numerous and 
the anastomoses very free. The lymphatic network is equally 
abundant, and mainly situated in the stroma of the gland around 
the acini. The larger lymphatics are supplied with valves like 
those of the veins. Occasionally colloid material has been found 
in the stroma and in the lymphatics. The capsule of the gland is 
a fibrous covering from which trabecular extend into the substance 
of the organ. 



576 



TEXT-BOOK OF PATHOLOGY. 



CONGENITAL DEFECTS. 

Occasionally one or another part of the gland is wanting, or in 
rare instances the entire organ. 

Accessory thyroid glands have been found in various situations. 
Sometimes small masses of thyroid tissue occur alongside of a nor- 
mal gland, either above it, in the neck ; or below it, behind the 
sternum and in the anterior mediastinum. In other cases the nor- 
mal thyroid is absent, but is represented by small masses in the 
situations named, or in other parts. In a few instances tumors at 
the base of the tongue and within the larynx and trachea have 
been found to be composed of thyroid tissue. 

DISTURBANCES OF CIRCULATION. 

Hyperemia of the thyroid gland is met with very frequently. 
It occurs in cases of cardiac failure, and in consequence of obstruc- 
tion of the large veins by mediastinal tumors, and the like. In 
these instances the thyroid may be considerably enlarged, and has 
a soft, doughy character. Slight enlargement of the thyroid of 
congestive character is found in perhaps a majority of the cases 
of chlorosis, and may be present in any form of anemia. In 
Graves' disease the thyroid may be very vascular, and the enlarge- 
ment of the gland may be in large part due to dilatation of the 
blood-vessels (see page 577). 

INFLAMMATIONS. 

Acute inflammation, or acute strumitis, may occur in 
the course of various infectious diseases, notably typhoid fever. 
Occasionally it arises without definite preceding disease. The 
gland enlarges and becomes rather tense. The termination is usu- 
ally in resolution, and this may occur very rapidly, suggesting 
that the enlargement of the gland is due largely to congestion and 
liquid exudation, rather than to cellular (inflammatory) infiltration. 

Acute suppurative strumitis, or abscess, occurs in con- 
sequence of embolism, in cases of infected wounds, endocarditis, 
or general pyemia. Sometimes the inflammation extends directly 
from local diseases, such as diphtheria. The abscess may rupture, 
or may undergo secondary changes — inspissation, calcification. 

STRUMA OR GOITER. 

Definition. — Goiter is the name applied to various enlarge- 
ments of the thyroid gland. It is a clinical rather than a patho- 
logic term. Sometimes a distinction is made between benign and 
malignant struma, the latter term including definite tumors of the 
thyroid gland. At the present time the term goiter is restricted 



DISEASES OF THE DUCTLESS GLANDS. 



577 



to enlargements of a hyperplastic character, which, though often 
resembling tumors, cannot be definitely classified among the tu- 
mors of the gland. 

Etiology. — Goiter occurs endemically in certain situations, as 
in Switzerland and other parts of Europe, and in parts of Michi- 
gan in this country. Sporadically it is met with in all parts of 
the world. Local conditions of some kind are doubtless among 
the fundamental causes, but the nature of these conditions is but 
little known. The drinking-water has always been suspected, and 
it seems likely that it has some influence, though it is certain that 
the magnesium and calcium salts have not the importance for- 
merly ascribed to them. Infectious causes have been suspected 
and micro-organisms have actually been described, but no satis- 
factory demonstrations have been made. 

Pathologic Anatomy. — Two principal varieties may be dis- 
tinguished : the parenchymatous and the vascular. 

Parenchymatous Goiter. — Parenchymatous goiter is a variety in 
which the glandular tissues or acini undergo more or less active 
hyperplasia. The gland is generally uniformly enlarged, but 
sometimes presents lobular or nodular elevations. The tissue is 
ordinarily somewhat elastic, like that of the normal thyroid, but 
may in other instances be very firm. Occasionally cystic forms 
occur, and a subvariety is sometimes distinguished by the term 
cystic goiter. 

Microscopically there may be found merely a uniform hyper- 
plasia of the glandular acini, without any notable change in the 
structure of the tissue. In other cases the acini are larger and 
more irregular than in the normal thyroid, suggesting the struct- 
ure of an adenoma, and the term struma adenomatosa is applied. 
In most instances the acini contain but small quantities of colloid 
material, as is the case in the normal gland. Sometimes, however, 
there is abundant production of colloid, and the acini are greatly 
distended ; the term colloid goiter may be applied in such instances 
(Fig. 264). In certain cases the walls of the acini are destroyed 
and the colloid of adjacent acini runs together, forming considerable 
cysts. In these instances the thyroid consists of numerous cystic 
excavations. Changes in the interstitial connective tissue of the 
gland may be comparatively slight, but may in other cases become 
conspicuous. The capsule of the gland may be thickened, and the 
stroma may predominate over the glandular elements. The term 
fibrous goiter has been suggested for such cases. 

Vascular Goiter. — This term is applied to enlargements of the 
thyroid gland characterized by marked dilatation of blood-vessels 
within the gland. The glandular tissues themselves may play no 
part in the process, or they may present changes similar to those 
described under parenchymatous goiter. The gland undergoes 
considerable and sometimes enormous enlargement, and may pul- 
37 



578 



TEXT-BOOK OF PATHOLOGY. 



sate actively. This form of goiter is met with as the important 
pathologic condition of manv cases of Graves' disease (see page 
582). 

Secondary Changes. — The thyroid frequently suffers second- 
ary changes in goiter. The hyperplasia of connective tissue 
between the acini has been referred to. Sometimes this becomes 
so considerable that the term fibrous goiter is warranted. Cystic 
formations have also been mentioned, the cysts referred to result- 




Fig. 264.— Colloid goiter, showing colloid material in the dilated acini. 



ing from the confluence of the dilated acini. The contents in such 
cases consist of colloid material or of more or less serous or hemor- 
rhagic liquid. Occasionally cysts result from hemorrhage in de- 
generated parts of the gland, with subsequent absorption of the 
blood, and exudation of serous liquid. The contents in such cases 
may be purely serous or may consist of brownish grumous matter 
containing abundant cholesterin. Very rarely secondary prolif- 
erative changes occur in the walls of the cyst, causing papilloma- 
tous projections. Calcification is a very common terminal change 
in degenerated goiters. It may occur in isolated areas, or may 



DISEASES OF THE DUCTLESS GLANDS* 



579 



cause a uniform hardening of the gland. Actual ossification has 
been observed. 

Mechanical Effects of Goiter. — The enlarged gland presses 
upon the adjacent structures more or less seriously. The trachea 
is most frequently compressed or dislocated from its median posi- 
tion. Pressure upon the large veins may occasion passive conges- 
tions and edema ; and less commonly pressure on the carotid 
artery may interfere with the circulation of blood in the brain. 
The nerves in the vicinity (vagus, recurrent laryngeal, and sym- 
pathetic) are likewise exposed to compression. 




Fig. 265.— Parenchymatous and vascular goiter, showing large, thick-walled blood-vessels. 



INFECTIOUS DISEASES. 

Tuberculosis may occur in the form of miliary tubercles or 
as small caseous nodules. 

Syphilis is met with in the form of gummata. 
Actinomycosis is a very rare disease of the thyroid gland. 



580 



TEXT-BOOK OF PATHOLOGY. 



TUMORS AND PARASITES. 

Tumors. — The term malignant struma is sometimes applied to 
tumors, and it is difficult in certain cases to draw a sharp line be- 
tween certain goiters and distinct new-growths (adenomata). 

The term adenoma, however, should be restricted to cases in 
which the proliferation of acini is more or less atypical, and in 
which the tumor is circumscribed, nodular, or otherwise distin- 
guishable from the pre-existing gland-tissue. Sometimes tumors 
of the thyroid having typically adenomatous characters give 
metastasis. 

Carcinoma may occur in the form of a nodular, or more diffuse 
tumor. Metastasis is frequent in cases of carcinoma, but also 
occurs in cases that present the appearances of an ordinary 
adenoma. The bones are frequently involved by metastatic de- 
posits. Extension from the thyroid to the adjacent organs is not 
infrequent. 

Sarcoma occurs in several varieties. Round-celled sarcoma 
and angiosarcoma are particularly malignant. 
Secondary tumors in the thyroid are rare. 

Parasites. — Echinococcus-cysts have been met with, but are 
very rare. 

GENERAL RESULTS OF THYROID DISEASE. 

The physiology of the gland has not as yet been fully deter- 
mined, though certain facts have become established. The old 
authors believed the gland to be active as a blood-making organ, 
and this is still maintained by some. It is, however, unlikely that 
this function is an important one. The frequent association of 
thyroid disease with certain general conditions (cretinism and 
myxedema) has led to experiments upon animals that have estab- 
lished certain important facts. 

The immediate removal, by operation, of the entire thyroid 
gland causes severe nervous manifestations resembling those of 
tetany followed by rapid death. Partial removal of the gland 
causes comparatively trivial consequences, but in cases in which 
total ablation has been practised, and in which a certain amount 
of thyroid influence has been kept up by injections of thyroid ex- 
tract or the feeding of thyroid gland, marked symptoms have been 
found to develop after a period of some months. Among these 
symptoms are pallor, edema of the skin, general weakness, dis- 
turbances of growth, and alteration of the cerebral functions 
(intellection, sensation, and motor poAver). This condition has 
been termed cachexia strumipriva, and its resemblance to cretin- 
ism and myxedema will be apparent from a reference to the symp- 
toms of those diseases. 



DISEASES OF THE DUCTLESS GLANDS. 



581 



Cretinism. — Cretinism is a peculiar disease, occurring with 
great frequency in certain parts of central Europe, especially in 
Switzerland, and not infrequently in 
other parts of the world. The thy- 
roid gland is sometimes atrophic, 
and sometimes goiterous, but in all 
cases diseased. The disease is not, 
as a rule, present at birth, but usu- 
ally develops soon after birth ; and 
the parents may be cretinoid or 
goiterous. Sometimes healthy par- 
ents have cretin children. The 
cretin remains physically and men- 
tally undeveloped ; the subcutane- 
ous tissue is flabby, abundant, and 
sometimes distinctly myxedematous 
(Fig. 266); the head is large; the 
lips and tongue enormously thick- 
ened, and the latter usually pro- 
trudes from the mouth ; the hairs 
of the body are little developed. 

Myxedema. — Myxedema is a 
disease that develops in later life ; 
sometimes after distinct diseases of 
the thyroid (goiter, gumma, tumors, 
etc.), but often without any mani- 
fest disease of thyroid, though 
atrophy and degenerations (calcifi- 
cation) may be disclosed by the 
post-mortem examination. There 
is a peculiar swelling of the eyelids and of the subcutaneous tissue 
of the face and neck, and subsequently the same change occurs 
elsewhere, involving the limbs and the entire body. The appear- 
ances at first suggest edema, but there is not the usual pitting on 
pressure, and the feeling conveyed to the hand is that of an infil- 
tration with some form of gelatinous tissue. This has been found 
to consist of a mucin-like substance, often associated with increase 
of the adipose tissue itself. The skin of the patient is pallid and 
exceedingly dry ; the hair falls out, and nervous symptoms are 
developed. Eventually intellection may be almost destroyed. 

The resemblance of these diseases to the symptoms produced 
by operative removal of the thyroid gland makes it certain that 
disease of the thyroid is the fundamental condition in cretinism 
and myxedema. This fact is still more clearly demonstrated by 
the numerous cures of these diseases following implantation of 
sheeps' thyroids in the peritoneal cavity, and especially the feed- 
ing of thyroid-gland tissue or extracts. 




Fig. 266.— Cretin, aged seven 
months ; showing facial features and 
myxedematous condition of hands 
arid feet (author's case at the Chil- 
dren's Hospital). 



582 



TEXT-BOOK OF PATHOLOGY. 



Graves' disease has been referred to in connection with 
goiter. The cardinal symptoms of this disease are enlargement 
of the gland, palpitation of the heart, exophthalmos, and mus- 
cular tremor. The pathology of the disease has not as yet 
been fully determined. It seems likely, however, from recent 
investigations that the thyroid disease, from whatever cause it may 
result, is the primary disorder. Removal of large parts of the 
gland has been found to control the symptoms of Graves' disease 
in a large number of cases, and the feeding of thyroid extract for 
a long period of time produces symptoms like those of Graves' 
disease : rapid action and palpitation of the heart, exophthalmos, 
and tremor. According to the view here expressed, the symptoms 
which together constitute Graves' disease are probably due to 
overproduction of thyroid secretion ; they are, in fact, the result 
of hyperthyroidism. The opinion, however, is held by others that 
Graves' disease is primarily an affection of the nervous system. 

THE SUPRARENAL BODIES. 

Anatomic Considerations. — The suprarenal bodies are 
composed of a cortical and a medullary portion, and are enclosed 
in a fibrous capsule from which septa extend into the substance. 
The cortical portion is composed of aggregations of polygonal 
cells which frequently contain fat-droplets. Three layers are 
distinguishable in the cortex : an outer zone, in which the cells 
are arranged in oval masses ; a middle zone, in which they form 
cylindrical columns extending toward the medullary ; and an inner 
zone, composed of irregularly anastomosing columns of cells. The 
cells of the middle zone are deeply pigmented and contain abun- 
dant granular and globular fat. The medulla of the gland consists 
of similar polygonal cells arranged in cords or irregularly anasto- 
mosing columns. Between these are found large venous channels 
and numerous non-medullated nerve-fibers, together with ganglion- 
cells. The fibrous septa of the gland contain blood-vessels and 
lymphatics. 

CONGENITAL ANOMALIES. 

Accessory suprarenal bodies may be found in the vicinity 
of the main body. Of peculiar interest are the portions of supra- 
renal tissue found in the capsule or cortex of the kidney. These 
"rests" may subsequently proliferate and form tumors of the 
kidney (see Tumors of the Kidney). 

Occasionally the suprarenal bodies are found in unusual situ- 
ations. 

DEGENERATIONS. 

Fatty degeneration is normal in adults. It affects the 
cortex, giving this layer a yellowish color. The substance of 



DISEASES OF THE GA STB 0- INTES TINA L TRACT 583 



the cortex may separate through the middle zone, forming a 
cavity suggesting a cyst. This is probably in part a post-mortem 
production. 

Pigmentation is observed in the cells of the medullary por- 
tion in persons of advanced age. 

Amyloid degeneration occurs in connection with amyloid 
disease of other organs. The suprarenal body becomes hard and 
of a grayish, translucent appearance. The degeneration affects 
the walls of the blood-vessels, from which it extends to the con- 
nective tissue. The glandular portions suffer pressure-atrophy. 
The cortex is more frequently involved than the medulla. 



INFECTIOUS DISEASES. 



Tuberculosis of the suprarenal body is the most important 
of its diseases. Miliary tubercles may be met with in cases of 
general tuberculosis, but a fibroeaseous 
form of the disease is more frequent and 
of much greater significance. The gland 
is enlarged, sometimes reaching the size 
of an egg ; it is hard and usually rather 
nodular, or irregular in outline. The 
capsule is thickened, and the substance 
of the gland is composed of dry, yellow- 
ish cheesy matter, or of a puriform mate- 
rial (Fig. 267). In the later stages the 
caseous or puriform matter may be ab- 
sorbed, and fibrous-tissue growth may 
convert the entire body into a shrivelled, 
hard mass of connective tissue. Some- 
times one gland alone is involved ; more 
frequently the disease occurs bilaterally. 
Tuberculosis of this form may be pri- 
mary, but usually is secondary to tuber- 
culosis of the lungs, intestines, or other 
organs. The general effects of this dis- 
ease will be discussed below (see Addi- 
son's Disease). 

Syphilis occurs in the form of 
gummata. Uniform fatty degeneration 
of the suprarenal body has been met with in congenital syphilis 




Fig. 267.— Caseous tuberculo- 
sis of the suprarenal body (Kast 
and Rumpel). 



CIRCULATORY DISTURBANCES. 

Hemorrhage is comparatively rare. It may occur in asso- 
ciation with hemorrhagic diseases, or severe anemias, especially 
leukemia. Sometimes it is caused by traumatism* or by obstruc- 



584 



TEXT-BOOK OF PATHOLOGY. 



tion of the venous circulation. The hemorrhage may be incon- 
siderable, or may be quite large. In the latter instances second- 
ary rupture of the hematoma may cause death by intraperitoneal 
hemorrhage, or a hemorrhagic cyst may result. 

INFLAMMATION. 

Inflammation of the suprarenal body is very rare. A simple 

and a hemorrhagic form have, however, been described. Abscess 
may occur in consequence of pyemia, or as a secondary condition 
following other forms of suprarenal disease. 

TUMORS. 

Sarcoma is the most frequent form of tumor. Melanotic, as 
well as unpigmented, varieties are met with. The tumor may 
reach considerable size, and may destroy the gland completely. 

Adenoma and carcinoma may arise from the cells of the 
acini. Histologically these tumors resemble the normal gland in 
their structure, and the term adenoma is perhaps more suitable 
than carcinoma. The tumor occurs as a nodular, irregular growth, 
often of a yellowish or brownish color ; it most frequently arises 
from the cortical portion of the gland. 

Gliomata of the suprarenal bodies have been described, but 
it is doubtful whether these tumors are true gliomata. Neuroma 
is a rare form of suprarenal disease. 

Secondary sarcoma and carcinoma are not infrequent. 

Tumors of the cortex of the kidney, having the structure of 
suprarenal tissue, are described under Tumors of the Kidneys. 

GENERAL EFFECTS OF SUPRARENAL DISEASES. 

The physiology of the suprarenal body is still obscure. It is 
quite generally believed, however, that this gland holds some rela- 
tion to pigment-formation, as well as to the circulation, either 
through the action of substances elaborated within the gland or 
through the nervous system. The last is suggested by the abun- 
dance of nervous tissue in the gland. 

Addison's disease, in which fibrocaseous tuberculosis of the 
suprarenal bodies is commonly present, is an affection character- 
ized by brownish pigmentation of the skin of exposed parts of the 
body (face, neck, and hands), and of the skin in the flexures of 
the joints, or in other parts subjected to pressure. The pigmenta- 
tion usually occurs in a mottled form at first, but soon becomes 
uniform. Brownish or purplish spots upon the mucous mem- 
branes (mouth) are not unusual. Besides pigmentation the char- 
acteristic symptoms are great weakness, disturbances of the stom- 
ach (vomiting), and cardiovascular asthenia. 



DISEASES OF THE ASTRO-INTESTINAL TRACT 



585 



Though fibrocaseoas tuberculosis of the suprarenal giand is 
discovered in many cases, Addison's disease may occur in associa- 
tion with other affections of the suprarenal, such as tumors ; and 
it may be absent despite the existence of tuberculosis or of other 
diseases of both of the glands. The absence of Addison's dis- 
ease in the latter cases has been explained by some writers by the 
assumption that the suprarenal disease had not existed long enough 
for the development of the symptoms of Addison's disease. Occa- 
sionally alterations in the sympathetic nervous system (semilunar 
ganglia and solar plexus) have been discovered when the supra- 
renal glands were apparently normal. No explanation of such 
cases can be made. It must be accepted at the present time that 
the suprarenal bodies are in some way concerned in the etiology 
of the disease. The disease of the gland need not, however, be 
of any special sort. 



CHAPTEE VII. 
DISEASES OF THE URINARY ORGANS. 
THE KIDNEYS. 
CONGENITAL ANOMALIES. 

Absence of one of the kidneys is frequently observed. Occa- 
sionally one kidney, instead of being completely absent, is atrophic 
or hypoplastic. The opposite kidney may undergo compensatory 
hypertrophy. Both kidneys may be wanting in certain monstros- 
ities. 

Congenital lobulation is quite common, and is usually bilateral. 
The kidney is divided into separate lobes by furrows of variable 
depth. Occasionally there is almost complete separation into 
numerous lobules. 

A few instances have been observed in which there was a 
third kidney, and usually in these cases two of the kidneys lying 
to one side of the spinal column were agglutinated. 

Fusion of the two kidneys may occur, and there may result a 
single large organ, with a double pelvis and ureter lying to one or 
the other side, or a horseshoe-kidney may be formed. In the latter 



586 



TEXT-BOOK OF PATHOLOGY. 



the two organs, which are generally displaced far downward, are 
united at their lower ends by a commissure passing across the 
spine just above the lumbosacral junction. The commissure may 
consist of normal kidney-tissue, or may be fibrous ; more com- 
monly the former. 

Congenital cysts and other congenital diseases will be referred 
to below. 

CHANGES OF POSITION. 

Congenital Malposition. — Not rarely one of the kidneys is 
displaced downward. It may even occupy the pelvis. In other 
cases it is displaced laterally or forward, and may be found imme- 
diately beneath the anterior abdominal walls. 

Acquired malpositions may result from pressure upon the 
organ, or from elongation of the peritoneal reflections covering the 
kidney and absorption of the perirenal fat. The right kidney is 
more frequently displaced than the left, and the condition is espe- 
cially common in women. Repeated pregnancies, the effects of 
tight lacing, and diseases or displacement of the liver are prom- 
inent causes. Movability or displacement of the kidney may be 
but a part of a general visceral descent (enteroptosis). 

Several grades of movability or displacement may be dis- 
tinguished. In the first, the perirenal fat is wanting, and the 
kidney is more movable beneath its peritoneal covering than is 
normal. This occurs in a large proportion of women, and usu- 
ally affects the right kidney. In more advanced grades the 
peritoneal reflection covering the kidney is elongated and con- 
siderable movability of the organ within the abdomen results. 
The kidney may be moved from side to side, downward as far as 
the pelvis in some cases, or upward to the normal position or under 
the ribs. In a third group of cases the kidney, lying within an 
elongated peritoneal pouch, is retained in an abnormal position 
by adhesions. 

Results. — Twisting of the pedicle may lead to serious circula- 
tory disturbances, and twisting of the ureter to retention of urine, 
sometimes causing hydronephrosis. Pressure of the displaced 
right kidney upon the duodenum may lead to dilatation of the 
stomach. 

CIRCULATORY DISTURBANCES. 

Anemia of the kidney may occur as a part of general anemia. 
The kidney is light in color and rather hard in the earlier stages ; 
but if the anemia persists degenerative softening and enlargement 
may ensue. 

Complete arrest of the blood-supply, produced experimentally, 
leads to rapid necrosis of the kidney, the organ becoming ashen- 



DISEASES OF THE URINARY ORGANS. 



587 



gray in color and of a homogeneous structure, so that the separate 
parts (cortex, medulla, pyramids) are indistinguishable. Near the 
cortex, where some circulation is maintained by the capsular ves- 
sels, fatty degeneration is observed. Somewhat similar changes 
are met with in circumscribed areas in diseases in which the circu- 
lation in branches of the renal artery is obstructed (see Embolism). 

Active hyperemia of the kidney is generally a part of acute 
inflammation. It may result from irritant chemical poisons or 
from the toxic action of infectious poisons. The kidney is en- 
larged, dark red in color, and on section the cortical substance is 
found to be swollen and marked by dark-red points — the Mal- 
pighian bodies. Sometimes punctate or linear hemorrhages may 
be observed. The urine is somewhat albuminous, and hyaline 
casts occur. It is difficult to draw a sharp line between this 
condition and acute nephritis. 

Passive hyperemia occurs in cardiac and pulmonary dis- 
eases which impede the circulation, or as a consequence of throm- 
bosis of the inferior vena cava or renal veins, or of other local 
causes obstructing the circulation in the renal veins. The kidney 
is enlarged and on section the cortex is found to be swollen, the 
substance of the kidney dark red in color, particularly in the 
pyramids in the vicinity of the large veins. The Malpighian 
bodies may be distinctly enlarged and dark red. 

Long-standing passive congestion leads to reactive hyperplasia 
of the interstitial connective tissue of the organ, and thus to a 
form of secondary interstitial nephritis. In these cases the kidney 
becomes contracted, the surface somewhat irregular, and the cap- 
sule ofttimes adherent. The organ may be intensely hard and pig- 
mented, and the term cyanotic induration is appropriate. 

The urine in passive hyperemia is, as a rule, deficient in 
quantity, and contains variable quantities of albumin and hyaline 
or granular tube-casts. 

Hemorrhage. — Punctate hemorrhages may occur in cases of 
intense active or passive hyperemia, the extravasation of blood 
occurring in the interstitial tissues, in the uriniferous tubules, or 
within the capsule of Bowman. Similar hemorrhages may be ob- 
served in acute or chronic nephritis. In these cases the extrava- 
sation of blood may occur by diapedesis or by actual rupture of 
the capillaries. Small hemorrhages may occur in the perirenal 
tissues in certain of the hemorrhagic diseases. Large hemorrhages 
occur within the kidney-substance only in cases of traumatism. 

Edema of the kidney results from obstruction of its venous 
circulation. The kidney becomes enlarged and soft, and the spaces 
between the convoluted tubules (the primary lymphatic spaces) are 
distinctly enlarged. There is associated congestion in these cases. 
Simple edema of the kidney may result from obstruction of the 
urinary outflow. 



588 



TEXT-BOOK OF PATHOLOGY. 



Thrombosis of the renal veins or their branches is rare. It 
causes intense hyperemia, hemorrhages, and edema, and later 
necrosis and degenerations. 

Embolism is very common in the branches of the renal 
arteries, especially in cases of disease of the aortic valves or 

atheroma of the aorta, Avith fibrin- 
ous deposits upon the atheroma- 
tous areas. The blood-vessels of 
the kidney correspond closely to 
the conception of terminal arteries, 
and infarction is therefore the usual 
result. In most cases the infarcts 
are light-colored areas having a 
wedge-shape, the base of the wedge 
being directed toward the capsule 
of the organ. A zone of reactive 
hyperemia or hemorrhage usually 
separates the infarct from the sur- 
rounding structures (Fig. 268). 
Less frequently the infarcts are 
purely hemorrhagic, the entire area 
being dark red in color. Minute 
emboli may lead merely to punc- 
tate hemorrhages within the kid- 
ney, or to ecchymotic extravasa- 
tions on the surface. 

The white or anemic infarcts 
undergo gradual necrosis and ab- 
sorption, with cicatrization or encapsulation, the contents in the 
latter case remaining as a dry detritus. The hemorrhagic infarcts 
more commonly soften, and finally terminate in cicatrization or in 
the formation of small cysts. In cases of infective embolism the 
anemic or hemorrhagic infarct may rapidly break down and form 
a metastatic abscess. 




Fig. 268.— Anemic infarcts of the 
kidney surrounded by a zone of hemor- 
rhagic infiltration (Kaufmann). 



INFLAMMATIONS. 



Inflammation of the kidneys may affect the substance {nephri- 
tis), the mucous membrane of the pelvis {pyelitis), or the capsule 
and peripheral portions {perinephritis). 



NEPHRITIS. 

Nephritis is the term given to a number of forms of degen- 
eration and inflammation of the substance of the kidney. The 
term Bright's disease is a clinical rather than pathologic one, being 
applied to various kinds of kidney-disease attended with albumin- 



DISEASES OF THE URINARY ORGANS. 589 



uria and dropsy. As a rule, however, the names B right's disease 
and nephritis are used synonymously. 

Nephritis may be acute or chronic ; and parenchymatous, dif- 
fuse, or interstitial. The term parenchymatous is applied to cases 
in which degenerative changes in the epithelium of the tubules or 
glomeruli are the most conspicuous feature ; the term diffuse is 
applied when exudative or proliferative changes affecting the con- 
nective tissues between the tubules and around the glomeruli and 
blood-vessels are associated in more or less equal proportions with 
the parenchymatous changes ; and the term interstitial nephritis is 
used in cases in which exudative and especially proliferative changes 
are alone conspicuous. 

Etiology. — Nephritis is due in the majority of cases to irritants 
which reach the kidney through the circulation. Intense acute 
nephritis may result from various poisons, particularly such as 
attack the parenchyma of organs, and are, therefore, known as 
parenchyma-poisons. Among these arsenic, mercury, phosphorus, 
cantharides, and turpentine are conspicuous. A second group of 
cases, and perhaps the largest of all, owe their origin to infections 
of various kinds. Nephritis is a common complication or sequel 
of scarlet fever, cholera, septicemia, diphtheria, and many other 
infectious diseases. In these cases the micro-organisms them- 
selves may reach the kidney through the circulation, as in typhoid 
fever, anthrax, or pneumonia, or the renal irritation may be caused 
by the toxins, as in cholera and diphtheria. Sometimes infectious 
nephritis is cryptogenetic, the portal of entrance of the micro- 
organisms being entirely obscure. In such cases streptococci, 
particularly, are operative. Certain chronic infections lead to 
nephritis by the action of the toxins or by slow nutritive disturb- 
ances. Such is the case in syphilis, tuberculosis, and malaria. 
Autointoxication occasions certain cases, as in the nephritis of 
gout and lithemia. 

In a small proportion of the cases nephritis results from irri- 
tants reaching the kidney through other channels than the circu- 
lation, as in pyelonephritis, a condition consequent upon inflam- 
matory processes ascending from the bladder and ureters, or as in 
nephritis secondary to extrarenal disease (psoas abscess). 

Low-grade renal inflammation may result from chronic conges- 
tion of the kidneys in consequence of cardiac and pulmonary dis- 
ease. In certain cases also it is likely that arterial disease affect- 
ing the renal arteries in common with other arteries of the body 
may initiate renal changes eventuating in a chronic interstitial form 
of nephritis. 

Pathologic Anatomy. — In considering the morbid anatomy the 
terms parenchymatous and interstitial are preserved, with the 
understanding that they are not strictly applicable to any given 
case. Pure parenchymatous inflammation does not exist, nor does 



590 TEXT-BOOK OF PATHOLOGY. 

interstitial nephritis occur without any parenchymatous change. 
Diffuse nephritis is considered under the heading parenchymatous 
nephritis. 

Acute Parenchymatous Nephritis ; Acute Bright's Disease. 

This results most frequently from infectious fevers and from 
toxic agents. It is more common in young persons than in the 
old. 

Acute Degenerative Nephritis. — The process in this 
condition may be almost purely parenchymatous in nature, and 
more nearly allied to pure degeneration than to inflamma- 
tion. The epithelium of the tubules, especially in the convo- 
luted portions, and to a certain extent also that covering 
the glomeruli, is swollen, cloudy, and considerably desqua- 
mated. Emigrated leukocytes, and occasionally red corpuscles, 
are found within the tubules and the capsule of the Malpighian 
bodies. The term acute catarrhal or desquamative nephritis is 
more or less appropriate in such cases. The kidney is enlarged, 
somewhat swollen, and generally rather pale in color. The 
changes are most marked in the cortex, which is thicker than 
normal, and by its light color contrasts strongly with the pyra- 
mids. The capsule strips easily. In most cases the affection is 
one of slight severity. 

Acute Glomerulonephritis. — In another group of cases, 
occurring most commonly in scarlet fever, the glomeruli are 
primarily attacked and most severely affected throughout the 
disease. Such cases are designated glomerulonephritis. The 



6 




Fig. 269.— Acute glomerulonephritis in diphtheria : a, albuminous exudate in Mal- 
pighian "body; b, convoluted tubule; c, vascular tuft or glomerulus covered with prolif- 
erated epithelium (Kaufmann). 

capillaries of the Malpighian tuft are distended, and the glom- 
erulus is filled with albuminous exudate, red and white blood- 
corpuscles and with proliferated and desquamated epithelial cells 



DISEASES OF THE URINARY ORGANS. 



591 



derived from the epithelium lining the capsule or that covering 
the Malpighian tuft (Fig. 269). Occasionally thrombosis occurs 
within the vessels, and hyaline degeneration may affect the cap- 
illary walls ; in other cases marked necrotic changes may occur 
in the epithelium covering the tufts of vessels and lining the sac. 

Acute diffuse nephritis is the ordinary form of acute 
Bright' s disease, and is the form in which either of the two pre- 
ceding are prone to terminate. The kidney is enlarged, and some- 
times congested and red in color ; at other times it is light-colored 
or even yellowish in consequence of the epithelial degeneration and 
the anemia caused by the epithelial swelling. On section the cor- 
tex is much increased in width, and when congestion exists it is 
more or less mottled, showing spots or streaks of reddish color, the 
intervening portions of the substance being grayish or yellowish in 
hue. In other cases the entire cortical substance is uniformly gray 
or yellow. The latter appearance is prone to occur in cases of con- 
siderable duration. In intense acute cases there may be punctate 
or linear hemorrhages, especially toward the surface of the organ, 
and the entire organ may be of a dark-red color. In all cases the 
capsule strips easily from the underlying substance. 

Microscopically the changes are most varied. In all cases 
there is more or less degeneration of the epithelium of the convo- 
luted tubules and of that in the Malpighian bodies. In the earlier 
stages the cells become swollen and granular (cloudy swelling), 
while in advanced stages they may be filled with dark granules 
or droplets of fat (fatty degeneration). On the other hand, 
cases of great intensity may be marked from the very first by 
complete necrosis of the epithelial cells. Similar changes may 
be met with in the epithelium of the Malpighian bodies, and the 
latter may be converted into granular masses in which the capil- 
lary tufts are more or less obscured. Associated with these purely 
parenchymatous changes are found evidences of interstitial involve- 
ment in the presence of masses of round cells between the tubules 
and in the vicinity of the Malpighian bodies. Active proliferation 
of the connective tissues is also observed, though less markedly, in 
the same situations. Certain cases are distinguished by their spe- 
cial tendency to hemorrhagic extravasations into and around the 
tubules and into the Malpighian bodies. To such the name acute 
hemorrhagic nephritis is sometimes applied. This variety is espe- 
cially common in intense septic or infectious cases, particularly 
such as are attended with minute embolism of the renal arterioles. 

Acute Interstitial Nephritis ; Suppurative Nephritis. 

Acute interstitial nephritis occurs in practically only one form, 
namely, in that which is characterized by the formation of purulent 
foci in the kidney. Acute interstitial changes, non-suppurative in 



592 



TEXT-BOOK OF PATHOLOGY. 



character, occur, as has been described, in association with paren- 
chymatous nephritis, but not as an independent affection. 

* Suppurative nephritis may result from metastatic involve- 
ment of the kidneys in cases of general septicopyemia, from ascend- 
ing inflammation in association with pyelitis, or from involvement 
of the kidney in cases of suppurative disease in the vicinity. 

Embolic suppurative nephritis leads to the formation of small 
foci of suppuration in the substance of the organ, especially toward 
the periphery. These may occur as mere points of yellowish color, 
or they may be surrounded by a considerable zone of hemorrhagic 
infiltration. The surface of the organ may be studded with small 
elevated points, and as the process advances larger foci may form 
by confluence. Microscopically the changes are found especially 
in the vicinity of the Malpighian bodies, in the small capillaries 
of which the micro-organisms primarily locate themselves. 
Hemorrhagic extravasation is usually marked, and the accumula- 
tions of leukocytes leading to suppuration are the characteristic 
feature. Degenerative changes may be seen in the epithelium of 
the vicinity, and, if the case has persisted for a certain length of 
time, parenchymatous changes may be quite extensive. 

In certain infectious fevers micro-organisms escape from the 
blood through the kidneys (pneumonia, typhoid fever, anthrax). 




Fig. 270.— Pyelonephritis, showing lines of ascending suppuration (Kaufmann). 



In such cases it is possible that the bacteria which have been ex- 
creted may cause infection in the lower parts of the uriniferous 
tubules. The occurrence of such nephritis is uncertain. 

Suppurative pyelonephritis occurs in cases of suppurative pye- 
litis, especially in consequence of impaction of calculi in the pelvis. 
In the earlier stages small linear areas of light color are seen in 
the pyramids and medulla, and microscopically these are found to 
be uriniferous tubules infiltrated with pus-cells (Fig. 270). In the 
later stages these may run together, forming purulent collections 
of considerable size. The superficial portions of the medulla and 
cortex are only secondarily involved, and the suppurative areas 



DISEASES OF THE URINARY ORGANS. 



593 



here assume a more rounded shape. Pyelonephritis may terminate 
by rupture of the abscesses into the pelvis of the kidney and the 
discharge of the pus with the urine ; by rupture on the surface of 
the kidney, causing perinephritic abscess ; or by inspissation and 
calcareous infiltration of the contents of the abscess. When dis- 
charge has taken place, or when inspissation occurs, induration and 
cicatrization of the diseased areas result. A considerable portion 
of the kidney may be thus converted into scar-tissue. 

Suppurative nephritis, following suppuration around the kidney, 
leads to the formation of superficial abscesses and erosions. 

CHRONIC NEPHRITIS. 

Chronic nephritis presents itself in varieties allied to the acute 
forms, and we may distinguish chronic parenchymatous and 
chronic interstitial nephritis. The former is practically always a 
diffuse process, presenting no such limitations to the epithelium 
of the tubules or to the glomeruli as are witnessed in the acute 
disease. Chronic interstitial nephritis is characterized mainly by 
hyperplasia of the connective tissue. 

CHRONIC PARENCHYMATOUS NEPHRITIS. 

Chronic parenchymatous nephritis in most cases results from 
acute attacks which have become chronic by continuation or repe- 
tition. It occurs after various infectious diseases, in consequence 
of alcoholism, or in an obscure manner, autointoxication probably 
accounting for some of the latter group of cases. 

Pathologic Anatomy. — The kidney is usually enlarged, and 
on section the cortical substance is often increased in width. The 
color is most frequently grayish or yellowish in consequence of the 
disease of the epithelium and of the anemia caused by the swell- 
ing of the cells. The pyramids may be quite red and swollen, 
or may be compressed and light in color. The capsule strips 
easily, and the substance of the organ is only moderately firm ; 
sometimes, indeed, it is quite soft. To this form of chronic 
parenchymatous nephritis the term large white kidney is often 
applied. In other cases the substance of the organ may be quite 
red in color, or may be mottled, light areas of yellowish or gray 
color alternating with congested portions. In such cases careful 
examination may show punctate or linear extravasations of blood, 
and the term chronic hemorrhagic nephritis is not inappropriate. 
The kidney is enlarged, as in the first variety, the cortex thick, 
and the capsule easily removed. In either case small cysts may 
form in the substance of the organ or upon the surface by disten- 
tion of the convoluted tubules or capsules of Bowman. 

In the later stages of chronic parenchymatous nephritis the 

38 



594 



TEXT-BOOK OF PATHOLOGY. 



degenerative processes in the epithelium become pronounced, and 
the organ may grow progressively lighter in color and more fatty 
in appearance. At the same time interstitial processes associate 
themselves, and the substance of the organ becomes more firm and 
the kidney is reduced in size. Attachments are formed between 
the substance and the capsule, which is no longer removable 
without laceration of the underlying substance. This terminal 
form of chronic parenchymatous nephritis has been designated as 
fatty contracting kidney, or as secondary interstitial nephritis, ac- 
cording to the amount of fatty parenchymatous change or of inter- 
stitial overgrowth present in the individual case (see page 595). 

Microscopically chronic parenchymatous nephritis is marked 
by striking degenerative changes in the epithelial cells of the con- 
voluted tubules, and to a less extent in those lining the capsule of 
Bowman and covering the Malpighian tufts (Fig. 271). The 




Fig. 271.— Chronic parenchymatous nephritis, showing marked involvement of the 
Malpighian body and considerable interstitial change. 

epithelium of the tubules is at first swollen and finely granular, 
the nucleus being obscured and the cells oftentimes becoming 
fused (cloudy swelling). In the more advanced stages of the pro- 
cess marked fatty degeneration of the cells is discovered, and they 
may break down completely, so that the lumen of the tubule is 
filled with fatty and granular detritus (Fig. 272). Extravasations of 
leukocytes or of red blood-corpuscles may take place, especially in 
the form known as hemorrhagic nephritis. Many of the tubules may 
be filled with tube-casts of hyaline or more frequently of granular 
appearance. The Malpighian bodies are usually simultaneously, 
though perhaps less markedly, affected. The epithelium in the 
latter is proliferated and degenerated, and the vascular tuft may 



DISEASES OF THE URINARY ORGANS. 



595 



present considerable hyaline degeneration. In the hemorrhagic 
variety the Malpighian body may be completely filled with extra v- 
asated blood. Side by side with these parenchymatous changes 
may be seen changes in the interstitial tissues. Notably, there 
are proliferation and thickening of the capsule of Bowman and of 




Fig. 272.— Chronic parenchymatous nephritis : a, convoluted tubules with cloudy swell- 
ing of the epithelium ; b, glomeruli, more or less degenerated ; c, atrophic tubules ; d, 
sclerotic interstitial tissue ; e, round-cell infiltration ; /, blood-vessel ; g, tube-casts in 
tubules (Kaufmann). 



the connective tissues between the tubules. In advanced stages 
these interstitial changes are always present, and in those cases 
known as secondary interstitial nephritis the connective-tissue 
hyperplasia is the predominating condition. The walls of the 
small blood-vessels of the kidney are usually thickened by hyper- 
plasia. 



CHRONIC INTERSTITIAL NEPHRITIS. 

Chronic interstitial nephritis leads to the formation of a con- 
tracted kidney. This may be a secondary form of nephritis fol- 
lowing chronic parenchymatous nephritis, or it may be primary, 
when it is often associated with diffuse arteriosclerosis. 

Secondary chronic interstitial nephritis is the terminal 
stage of certain cases of chronic parenchymatous nephritis, and 
results from a continuous hyperplasia of the interstitial tissues, 
with degeneration and atrophy of the parenchyma. The organ is 
reduced in size, and may be quite irregular upon the surface, the 
irregularity taking the form of large depressions or of fine granu- 
lations. The capsule strips with difficulty, portions of the kidney- 



596 



TEXT-BOOK OF PATHOLOGY. 



substance remaining attached. On section the kidney is found 
to be firmer than normal, and is of light color, often yellowish 
(fatty) in hue. The cortex may be nearly the normal thickness, 
or may be considerably reduced. The small blood-vessels of the 
substance of the organ may be patulous and evidently sclerotic. 

Microscopically the epithelium of the tubules is granular, fatty, 
or atrophic, and the cells are found detached in great numbers and 
occupying the lumen of the tubules. The tubules themselves may 
be compressed by surrounding interstitial overgrowth, or may be 
distended even to the formation of cystic dilatations. The capsule 
of Bowman is greatly thickened, and the Malpighian bodies may 
be much distorted and compressed. 

Primary Chronic Interstitial Nephritis ; Red Granu- 
lar Kidney ; Arteriosclerotic Nephritis ; Gouty Nephri- 
tis. — All of these terms have been applied to a form of inter- 
stitial nephritis probably produced by irritants conveyed through 
the circulation. It occurs in consequence of alcoholism, syphilis, 
gout, chronic plumbism, and chronic cachexias of other kinds. It 
is not rarely associated with diffuse arteriosclerosis. A certain 
amount of interstitial nephritis of this variety is a natural lesion 
of old age. 

Pathologic Anatomy. — The kidney is usually decreased in size, 




Fig. 273.— Chronic interstitial nephritis ; granular kidney (Orth). 

and sometimes may be very much contracted. In other cases 
the reduction in the dimensions is inconsiderable, and the size- 
may even be increased. The surface is irregular, and, on removal 



DISEASES OF THE URINARY ORGANS. 597 

of the capsule, is found to be finely granular or irregularly tabu- 
lated (Fig. 273). The capsule itself strips with difficulty. Small 




Fig. 274.— Chronic interstitial nephritis : great increase of connective tissue around the 
glomeruli, renal tubules, and blood-vessels. 

cysts may be seen upon the surface. On section the substance is 
firm, and may sometimes be almost cartilaginous in consistence. 




Fig. 275.— Chronic interstitial nephritis (from a photograph by Dr. Wm. M. Gray). 

The cortex is narrow, often being reduced to a quarter or one-sixth 
its normal width ; while the pyramids may be increased in size or 
contracted like the cortex, and not rarely show dense white sclero- 
tic tissue radiating from the apices. In gouty cases deposits of 
urates may be observed in the same situation. The color of the 
kidney varies, but is usually grayish-brown or gray. The blood- 



598 



TEXT-BOOK OF PATHOLOGY. 



vessels in the substance of the organ are usually patulous and 
their walls visibly thickened. 

Microscopically, chronic interstitial nephritis is characterized 
by great hyperplasia of the connective tissue surrounding the Mal- 
pighian bodies and the convoluted tubules, and by hyperplasia of 
the walls of the blood-vessels (Fig. 274). The overgrowth of 
connective tissue may be irregular in its distribution, and may 
vary greatly in amount. In beginning cases there is only moder- 
ate thickening of the capsules of Bowman and of the intertubular 
tissues and walls of the blood-vessels. In the most pronounced 
cases the kidney-substance is almost wholly transformed into 
fibrous tissue of dense sclerotic character (Fig. 275). The epithe- 
lium undergoes progressive atrophy, the cells shrinking in size and 
becoming granular and loosened from the basement-membrane. 
Hyaline or granular tube-casts may be found within the tubules, 
and the latter are compressed by contraction of the new-formed 
connective tissue, or in other cases dilated by the disappearance of 
the epithelium. 

Pathologic Physiology of Nephritis. — The effect of acute 
or chronic nephritis varies greatly in individual cases. Profound 
systemic disturbances in acute cases are doubtless often the result 
of the action of toxic substances, which caused the nephritis, rather 
than of the disease of the kidneys itself. In uncomplicated cases 
of acute or chronic nephritis the influence upon the general metabo- 
lism is seemingly slight. Investigations have not as yet shown 
any decided increase in the metabolic consumption of the tissues, 
and no specific disturbances of metabolism of any sort have been 
discovered. It is very likely, however, that extensive disease of 
the kidneys does exercise some influence, since these organs un- 
doubtedly have actual glandular functions and are not merely 
passive agents for the filtration of the blood and the excretion of 
urine. The peculiar intoxication which occurs in nephritis, and to 
which the name uremia (q. v.) is applied, has received no satis- 
factory explanation. It is probable that substances normally 
excreted in the urine are retained in the blood and accumulate to 
such an extent that intoxication results. It is also likely that sub- 
stances which are normally elaborated by the kidneys and excreted 
in altered forms remain in the blood and occasion disturbances. 
During the progress of uremia there seems undoubtedly to be 
active tissue-consumption, but accurate studies are wanting. 

Gastro-intestinal symptoms are frequent in renal disease. In 
a notable proportion of cases the gastric secretion has been found 
deficient, and this may account for some of the disturbances. 
Putrefactive processes in the intestines have also been demon- 
strated in some cases, being evidenced by the increased quantity 
of ethereal sulphates in the urine. In the later stages of nephri- 
tis, and especially in uremia, severe gastro-intestinal disorders 



DISEASES OF THE URINARY ORGANS. 



599 



sometimes develop. These have been explained by the assump- 
tion that urea is excreted through the gastro-intestinal mucous 
membrane, and undergoes ammoniacal decomposition within the 
digestive tract. The ammonia formed by this decomposition is 
supposed to be the immediate cause of the gastro-intestinal dis- 
turbance. 

The urine in nephritis is of the greatest interest. In acute 
cases, and sometimes in chronic forms it suffers notable change of 
appearance by admixture of blood. In other instances the color 
and physical properties are to a large extent dependent upon its 
amount. As a rale, the quantity of urine is decreased. The 
nitrogenous elimination is of particular interest. In acute cases, in 
which the quantity of urine is greatly deficient, there is undoubt- 
edly an insufficient excretion of nitrogen from the urine ; subse- 
quently the nitrogenous element may be excreted in increased 
quantities. In acute nephritis without marked diminution in the 
quantity of urine, the nitrogenous elimination may remain satis- 
factory. In chronic nephritis the elimination of nitrogen in the 
urine may be reduced, both in the parenchymatous and interstitial 
forms of nephritis. The amount of urea is very commonly de- 
creased ; in part this may be compensated for by increased elimi- 
nation through the skin and intestines. Nitrogen retention is 
not invariable, and from time to time periods of increased elimi- 
nation may occur. The uric acid is usually decreased in quantity, 
but may be entirely normal in any form of nephritis, and may in 
some instances be temporarily increased. Ammonia is present in 
normal quantities. During uremia it may be increased. Xanthin 
may be present in increased quantities, and creatinin is reduced in 
quantity. 

The urine in nephritis presents two striking peculiarities : the 
presence of albumin, discoverable by chemical examination, and 
the presence of tube-casts. Albuminuria is an almost constant 
symptom, though occasionally, in chronic interstitial nephritis, the 
amount may be so small that it is not detected by the cruder tests. 
The more delicate methods will probably detect albumin in every 
case. Serum-albumin is the more important form, but globulin 
occurs in small amounts in every case. In hemorrhagic forms of 
acute or chronic nephritis and in cases complicated by amyloid 
degeneration globulin may be found in considerable quantity. 

The tube-casts met with in nephritis are casts formed within 
the convoluted tubules, or more rarely in other parts, and are com- 
posed of albuminoid substances and possibly sometimes of fibrin. 
They are formed partly of materials which have accumulated in 
the tubules by exudation, partly of the granular detritus of the 
degenerated epithelium, or of red and white blood-corpuscles. 
We may distinguish a number of varieties, viz., hyaline, cellular, 
crystalline, and granular casts and cylindroids. 



600 



TEXT-BOOK OF PATHOLOGY. 



Hyaline casts are clear, rounded bodies having a diameter of 
from 0.01 to 0.03 mm. and a variable length. Sometimes they 
are quite short ; at other times they extend across several fields 
of the microscope. They may be straight, or spiral or contorted. 
Sometimes they are so transparent and light colored that they are 
scarcely visible, or, on the other hand, they may be of a denser 
structure and less transparent. Hyaline casts are frequently met 
with in simple congestion of the kidney and in icterus unassociated 
with discoverable nephritis. They are most abundant in acute 
parenchymatous nephritis, but are met with also in chronic 
parenchymatous and interstitial nephritis. A form of hyaline 
cast known as the waxy cast is met with, sometimes in acute, but 
more commonly in chronic nephritis (Fig. 276). It is distin- 




Fig. 276.— Waxy hyaline casts. Fig. 277.— Blood-casts, composed wholly 

of red or white corpuscles, or hyaline sub- 
stance covered with blood-corpuscle. 



guished by the moulded, wax-like appearance and by its apparent 
rigidity. 

Cellular Casts. — The most frequent form is that in which the 
surface of a hyaline or granular cast is covered with epithelial 
cells that have detached themselves from the tubules. The 
entire surface may be covered, or there may be but a few cells 
here and there. This form is found especially in acute parenchy- 
matous nephritis. Leucocytic casts are moulds of the tubules com- 
posed of masses of leukocytes. They are found especially in 
purulent pyelonephritis. Occasionally leukocytes are found upon 
the surface of other casts. Blood-casts, composed of red blood- 
corpuscles, or of blood-pigment formed by disintegrated red cor- 
puscles, are frequently observed in acute and chronic hemorrhagic 
nephritis (Fig. 277). 

Crystalline Casts. — Moulds of the tubules, composed of uric 
acid or oxalate of lime, are sometimes observed in chronic nephri- 



DISEASES OF THE URIXARY ORGANS. 



601 



tis, when there is a tendency to the deposition of the crystals 
named (Fig. 278, A). Similar formations may be met with in the 
urine of the new-born independently of nephritis (see page 607). 
Granular casts may be light or dark, according to the amount 




Fig. 278— A, Tube-casts, composed of uric-acid crystals ; B, granular and fatty casts and 
two compound granular cells." 



and character of the granular material. They are composed of 
substances derived from broken-down epithelial cells, and are 
especially common in chronic nephritis, though they may occur in 




Fig. 279.— Cylindroids : a and b, cast-like forms ; c, filamentous forms. 

quite acute cases. Sometimes, instead of granular matter, the 
debris of the epithelial cells occurs as oil-drops, and the term 
fatty casts) is appropriately applied (Fig. 278, B). The diameter 
and length of granular casts vary considerably. As a rule, the 
diameter is about the same as that of the hyaline casts, but the 
length is rarely as great. 



602 



TEXT-BOOK OF PATHOLOGY. 



Cylindroids are formations resembling casts more or less 
closely. Sometimes they appear as thread-like formations, rounded 
or flat, and occurring singly or in twisted bunches. In other 
cases they may be quite similar to hyaline casts, though distin- 
guished by a long, tapering end or tail (Fig. 279). Cylindroids 
occur in conditions of renal irritation not sufficient to constitute 
nephritis, as well as in cases of genuine nephritis. They are also 
supposed to be produced in the tubular glands of other parts of the 
genito-urinary tract, as in the glands of Cowper. 

Other Constituents of the Urine. — Various cellular constituents 
are found in nephritis. In acute and in chronic hemorrhagic 
nephritis white and red blood-corpuscles are frequently observed ; 
and epithelial cells are more or less abundant in all forms of 
parenchymatous nephritis. In the acuter varieties swollen and 
granular rounded cells are observed ; in the more chronic forms, 
particularly when fatty degeneration is pronounced, epithelial 
cells or leukocytes densely filled with dark granular or globular 
fat are conspicuous. The term compound granule-cell has been 
applied to these cells. 

Results of Nephritis. — Nephritis leads to notable changes 
in the entire organism, and particularly in the vascular system. 

Cardiac Changes. — In acute nephritis there may be associated 
acute degenerative or inflammatory lesions of the heart-muscle, and 
cardiac dilatation may occur. These, however, are usually results 
of the infectious or toxic cause underlying the nephritis, rather 
than results of the nephritis itself. When parenchymatous nephri- 
tis becomes subacute or chronic, hypertrophy of the heart (notably 
of the left ventricle) takes place, and this reaches extreme propor- 
tions in chronic interstitial nephritis. The cause of the hyper- 
trophy of the heart has occasioned much controversy. It seems 
likely that it is in large part the result of irritation and over-stimu- 
lation of the heart-muscle by substances retained in the blood, 
instead of being excreted. The obstruction to the circulation 
occasioned by thickening of the walls of the renal vessels is of 
little moment ; and the theory that the cardiac hypertrophy is 
due to a hydremic condition and increased quantity of blood, 
in consequence of retention of water in the system, is nega- 
tived by the fact that such hydremic excess of blood is certainly 
absent in many cases. Associated arteriosclerosis is undoubtedly 
one of the important factors in the production of cardiac hyper- 
trophy. 

Arteriosclerosis. — The arteries are frequently sclerotic in cases 
of chronic nephritis. In part this is due to the direct action of 
toxic products of improper metabolism occurring in Bright's 
disease ; in part it is a coincidental or an antecedent condition. 

Acute inflammatory lesions of the serous membranes, and to a 
less extent of the mucous membranes, sometimes occur in Bright's 



DISEASES OF THE URINARY ORGANS. 



603 



disease. Acute endocarditis, acute pericarditis, and pleurisy are 
the most frequent conditions. Of the inflammatory conditions of 
the mucous membranes, tonsillitis and pharyngitis are not infre- 
quent. Enteritis, even of ulcerative type, may occur, especially 
in chronic nephritis. This, in part, seems to result from vicarious 
excretion of irritant matters from the intestinal mucosa. 

Edema, or dropsy, is a frequent manifestation of nephritis. It 
is most frequent in the parenchymatous forms, particularly in such 
as occasion changes in the glomeruli and other vascular portions 
of the kidney. The important etiologic factor is doubtless disease 
of the blood-vessels. In chronic interstitial nephritis dropsy is 
rarely observed until the late stages, when manifest arterial dis- 
ease and failing circulation from cardiac weakness have super- 
vened. The edema usually begins in the loose subcutaneous tissues 
of the eyelids and hands, but extends to all parts of the body, 
causing anasarca. Internal edema, and especially edema of the 
lungs, may be met with. 

Uremia is the name applied to certain clinical manifestations 
probably caused by the retention of toxic substances in the blood 
which ordinarily are excreted with the urine. The nature of the 
substance or substances in question remains obscure. Neither 
urea, potassium nor ammonium salts, uric acid, nor various other 
constituents of the urine alone produce ursemic manifestations; 
though the injection into animals of some of these may cause toxic 
symptoms, such as convulsions or coma. It may be that uremia is 
caused by the conjoined action of a number of such toxic bodies, 
but it is not improbable that the poisons are substances as yet un- 
discovered. The theory that uremia is due to edema or anemia 
of the brain may be definitely abandoned. 

ATROPHY AND HYPERTROPHY. 

Atrophy of the kidney may be congenital (hypoplasia), or may 
occur in old age (senile atrophy). In the latter case the kidney is 
small, hard, and usually darker in color than normal. The irreg- 
ular atrophy of the parenchyma leads to irregularities upon the sur- 
face of the organ. The capsule may be thickened, and not rarely 
the perirenal fat is abundant, and considerable fatty deposit occurs 
beneath the mucous membrane of the pelvis. 

Microscopically the renal cells are small in size, somewhat 
dark, and granular. They may disappear entirely from the 
tubules in places, and the intertubular tissue and the basement- 
membrane are correspondingly thickened. The Malpighian bodies 
may be converted into contracted fibrous areas. In some cases 
the interstitial processes become so pronounced that the changes 
in the kidney become those of interstitial nephritis. These cases 



604 



TEXT-BOOK OF PATHOLOGY. 



are particularly met with in persons of advanced years having 
arteriosclerosis (see Chronic Interstitial Nephritis). 

Hypertrophy may affect one kidney when its fellow is con- 
genially wanting, has become diseased, or has been removed. 
Under these circumstances the remaining or healthy organ some- 
times undergoes considerable hypertrophy. The appearance is 
that of a much enlarged but otherwise normal kidney. 

Microscopically there may be simply increase of the size of the 
tubules, or in cases in which the compensatory hypertrophy has 
begun before the completion of development there may be actual 
increase in the number of tubules and Malpighian bodies. 

DEGENERATIONS. 

Parenchymatous degeneration, or cloudy swelling, 

occurs in the kidneys in consequence of the action of various 
poisons, infectious or chemical. It is met with in practically all 
cases of diphtheria, scarlet fever, and cholera, and less commonly 
in many other infectious diseases. Among the poisons the various 
parenchyma-poisons (q. v., Part I) are all capable of attacking the 
kidney and producing cloudy swelling. In case of either toxic or 
infectious degenerations, however, the process is prone to become 
more serious, and to terminate in acute parenchymatous nephritis. 
No sharp dividing-line can be drawn between the two conditions. 

The kidney is somewhat increased in size, is softer than nor- 
mal, and on section the cortex is yellowish or of light-grayish 
color (Fig. 280). The Malpighian bodies may be prominent as 




Fig. 280.— Parenchymatous degeneration of the kidney, from a case of cholera (modified 
from Kast and Rumpel). 

red spots lying in the light-colored renal tissue. The pyramids 
are often congested, and contrast strongly with the cortical sub- 
stance. 

Microscopically, fine granulation of the cells of the convoluted 



DISEASES OF THE URINARY ORGANS. 



605 



or other tubules is the striking feature. The nuclei of the cells 
are obscured, and at times all of the cells of the tubule apparently 
become fused. Exudative changes and hyperplasia of the inter- 
stitial tissues are wanting in a purely degenerative condition. Fre- 
quently the kidney is restored to the normal condition, but, on 
the other hand, acute Bright's disease or fatty degeneration may 
ensue. 

Fatty Degeneration. — This occurs in consequence of the 
last-described condition, or independently in consequence of gen- 
eral anemia and systemic disorders, as in progressive pernicious 
anemia and tuberculosis. Fatty degeneration of the kidney fre- 
quently occurs in the course of pregnancy, when it is due to dis- 
turbance of the circulation in the kidneys or possibly to obstruc- 
tion of the ureters. In these cases the process usually advances 
to the condition of diffuse nephritis. 

In pure fatty degeneration the kidney is about the normal size, 
or often smaller than normal ; is soft ; and on section the cortex 
has about the normal width. The color is uniformly yellowish or 
mottled, certain areas being yellowish in color and others normal 
or perhaps hyperemic. Usually the surface of the kidney is 
smooth, but sometimes localized spots of degeneration may become 
depressed and give rise to irregularities. 

Microscopically the epithelial cells are granular, or filled with 
oil-drops (Fig. 281). Not rarely the cells are loosened and lie 



••L tf>', ' <*»*# «, °»»« 



S.V.. 



Fig. 281.— Fatty degeneration of the epithelium of the tubules : stained with osmic acid 

(Simmonds) . 



free within the lumen of the tubules. The basement-membrane 
and interstitial tissues may be somewhat thickened, either appar- 
ently or actually. 



606 



TEXT-BOOK OF PATHOLOGY. 



Fatty infiltration is an unimportant condition. In the 
atrophic kidney of old age and in the contracted kidneys of 
chronic nephritis fatty infiltration of the areolar tissue beneath the 
mucosa of the pelvis is frequently observed. Fatty infiltration of 
the epithelial cells may occur under normal conditions, or in cases 
in which the blood is surcharged with fat (lipemia) and in which 
the kidneys are actively engaged in its excretion. Fatty infiltra- 
tion of the perirenal cellular tissues occurs in general obesity, and 
sometimes as a localized affection in cases of advanced renal dis- 
ease, particularly atrophy. 

Calcification may occur in diseased areas of the kidneys, as 
in sclerotic Malpighian bodies, in old infarcts and the like. Occa- 
sionally calcification occurs in the epithelial cells themselves, 
particularly in such as have undergone necrosis. 

Glycogenic infiltration of the kidneys occurs in diabetes. 
It affects the epithelial cells, particularly those in the portions of 
the organ lying between the medulla and the cortex. The kidney 
is usually increased in size, the cortex broader than normal, and 
the consistency increased. The substance may be lighter colored 
and of homogeneous appearance. Microscopically the epithelial 
cells, particularly those of the tubes of Henle, are found to be 
altered in character, the normal granular condition of the proto- 
plasm having disappeared. The glycogenic nature of the infil- 
trating substance is recognized by the dark-brown color obtained 
by staining fresh sections with iodin. 

Amyloid degeneration occurs in the kidneys under the same 
conditions as in the liver and spleen. It is most frequent in cases 
of chronic tuberculosis of the lungs, and occurs in cases of long- 
standing suppuration connected with bone, in syphilis, and as a 
result of other cachexias. The kidney is enlarged, sometimes to 
twice its normal bulk, is harder than normal, and on section the 
substance is found light grayish in color. It may be uniformly 
grayish or waxy ; or, on the other hand, it may be mottled, gray- 
ish areas alternating with portions of yellow color, the latter being 
due to fatty degeneration. Amyloid degeneration begins in the 
small blood-vessels, particularly those of the Malpighian tufts, and 
spreads to the connective tissues of the organ, but does not involve 
the epithelium. 

Microscopically the glomeruli may present spots of hyaline or 
homogeneous appearance in which the capillaries seem completely 
disorganized, and the entire glomerulus may be transformed into 
a transparent or translucent mass (Fig. 282). The capsule is 
thickened and ofttimes simultaneously diseased. The tubules 
habitually contain hyaline casts. The organ becomes more or 
less anemic from obstruction of the capillaries, and sooner or later 
fatty degeneration of the epithelial cells takes place. Inflamma- 
tory processes are usually wanting, but nephritis may become 



DISEASES OF THE URINARY ORGANS. 



607 



associated with amyloid degeneration, and the latter process may 
occur in kidneys primarily the seat of nephritis. The urine in 
amyloid disease is albuminous and scanty ; the proportion of 
serum-globulin is excessive. Not rarely it contains hyaline 
casts which respond more or less distinctly to the color-tests for 




Fig. 282.— Contracted and amyloid kidney (from a photograph by Dr. Wm. M. Gray). 

amyloid substance, but these are not diagnostic, and it is doubtful 
whether they are in reality composed of amyloid material. 

CONCRETIONS IN THE URINIFEROUS TUBULES. 

Various calcareous concretions, or " infarcts," occur in the uri- 
niferous tubules, particularly in the large collecting tubules near 
their termination at the apex of the pyramids. Collections of 
urates, particularly urate of ammonium, are frequently seen in 
the form of radiating lines of light-grayish, yellowish, or reddish 
color, marking the pyramids near the apices in new-born infants. 
These consist of crystalline concretions filling the large uriniferous 
tubules, and have been considered as a valuable medicolegal indi- 
cation that the infant had breathed. They are not, however, suf- 
ficient proof. Sometimes the concretions are passed with the urine, 
and are discovered as large casts of conglomerated crystals. Less 
frequently other forms of crystals are met with in the infarcts of 
the new-born. Similar concretions occur in gouty individuals, par- 
ticularly in aged persons, and calcium salts may be deposited when 
the blood is surcharged with them in consequence of diseases of 



608 



TEXT-BOOK OF PATHOLOGY. 



the bones. Triple phosphates may be found as a consequence of 
obstruction of the urinary passages and stagnation of urine. 

Concretions composed of bilirubin may be formed in extreme 
jaundice, and particularly in the jaundice of the new-born. In- 
farcts composed of hemoglobin may be seen in cases of hemo- 
globinuria due to infectious and toxic causes. 

INFECTIOUS DISEASES. 

Tuberculosis. — Tuberculosis may occur in the kidney in the 
form of minute, grayish- white miliary tubercles as part of a 
general hematogeneous tuberculosis. A second form, which is 
also hematogenic, is known as chronic local tuberculosis. In this 
form the substance of the kidney near the cortex, or sometimes 
that adjacent to the pelvis, is occupied by masses of cheesy tuber- 
culous tissue, and there may be secondary miliary tuberculosis 
near by. Softening is prone to occur, and the tuberculous focus 
may discharge into the pelvis of the kidney, leaving a necrotic 
cavity, The entire organ may be transformed in this manner. 
Tuberculosis of the kidney may also result from ascending infec- 
tion, being secondary to tuberculosis of the seminal vesicles of the 
bladder, of the ureters, and of the pelvis of the kidney. The pro- 
cess first involves the discharging tubules at the apices of the 
pyramids and spreads outward toward the cortex. Cheesy foci are 
formed, which may soften and discharge into the pelvis, as in the 
case of chronic local tuberculosis of the kidney. It is difficult to 
determine whether tuberculosis of the kidneys is more frequently 
the result of urogenital tuberculosis primarily affecting the parts 
below, or the cause of the latter. Primary affection of the kid- 
ney is certainly more common than many have been disposed to 
admit. 

Syphilis. — In the earlier stages of syphilis there may possibly 
be acute nephritis similar to that of other infectious diseases. Syph- 
ilis of long duration may lead to amyloid degeneration of the kid- 
ney, or to chronic interstitial nephritis. In the latter case con- 
tractions of fibrous tissue leading to marked lobulation are rather 
characteristic. Syphilitic gummata are rare, but have been met 
with, and in their healing lead to marked scar-formation. 

TUMORS. 

Fibromata and lipomata may occasionally be met with in 
the kidney in the form of small rounded nodules. In association 
with calculous pyelitis and other conditions of the kidney leading 
to atrophy, the fatty tissue surrounding the kidney may be in- 
creased to such an extent as to constitute practically a fatty tumor. 

leiomyoma is an occasional growth of the kidney. 



DISEASES OF THE URINARY ORGANS. 



609 



Congenital Adenoma. — Under the name of struma aberrata 
suprarenalis has been described a form of tumor of the kidney 
which results from splitting off of a remnant of the suprarenal 
capsule and its incorporation in the kidney, where it subsequently 
grows. The tumor presents the appearance of a small lipomatous 
growth beneath the capsule of the kidney, or, more rarely, it may 
attain considerable size. Histologically it consists of epithelial 
cells arranged in tubules similar to those of the cortical portion 
of the suprarenal capsule. These undergo considerable fatty 
infiltration, and almost the entire tumor may be fatty. Occasion- 
ally active proliferative changes occur in the epithelium, and a 
malignant character is assumed. 

Sarcoma of the kidney is the most frequent malignant tumor. 
It may occur congenitally, or in later life. The size and general 
appearance vary considerably, but for the most part the structure 
is soft and grayish or sometimes quite red. Extravasations of 
blood or hemorrhages into the tumor are not uncommon. There 
may be a distinct capsule, or the growth may be an infiltrating 
one. Cystic softening is not infrequent. 

Microscopically the appearance varies considerably, and the 
growth may be composed of round cells, spindle cells, or cells of 
various shapes. Not rarely a certain number of striped muscle- 
fibers are found, and to such growths the term rhabdomyosa?'coma 
has been applied. In other cases there may be embedded in the 
sarcomatous tissue glandular acini composed of cylindrical or irreg- 
ular epithelium, and to such the name adenosarcoma is applicable 




Fig. 283.— Adenosarcoma of the kidney (modified from Kast and Rumpel). 



(Fig. 283). Occasionally myxomatous tissue, smooth muscle-fibers, 
or even islets of cartilage are found. The multiform character of 
sarcoma of the kidney suggests an embryonal origin, and it is not 
unlikely that inclusions of the primitive Wolffian body are the 
starting-point of the disease. 

Adenoma of the kidney is rare. It originates in the convo- 
luted tubules, and presents itself in the form of more or less 

39 



610 TEXT-BOOK OF PATHOLOGY. 

nodular masses. Microscopically the appearance is that of a 
tubular adenoma. Proliferative changes occasionally affect the 
uriniferous tubules in interstitial nephritis, and give rise to small 
areas of adenomatous appearance. In such cases, however, the 
appearances are not those of a tumor in the strict sense. 

Papuliferous cystic adenoma is sometimes observed. It 
occasions tumors of small or large size with fibrous capsules and 
cystic excavations in which the lining epithelium is elevated in 
a papillomatous manner. 

Carcinoma is a rare primary tumor of the kidney, and occurs 
in persons of advanced years. The growth begins in the cortical 
substance or in the medulla, and presents itself as a soft white or, 
in case of hemorrhage into it, red tumor. 

Microscopically it is found to be a glandular carcinoma pre- 
senting acini composed of epithelial cells of various shapes. 
Metastasis is rare. 

Secondary Tumors. — Among the secondary tumors of the 
kidney are both sarcoma and carcinoma. 

In the same group may be included the lymphomatous infiltra- 




Fig. 284.— Lymphoid infiltrations between the renal tubules ; from a case of leukemia. 

Hons of leukemia (Fig. 284). In this disease the kidney is often 
enlarged, and on section is found to be uniformly white or mottled 
in color, the light-colored areas representing masses of lymphoid 
cells. Most of these have doubtless been deposited from the cir- 
culation, but there is also evidence of local multiplication. 

Cysts of the kidney are of various forms. In the course of 
chronic nephritis, especially the interstitial form, cystic dilatations 
of the convoluted tubules and Malpighian bodies are observed. 
These appear as small or large rounded bodies lying immediately 
beneath the capsule, and on section are found to contain serous liquid, 



DISEASES OF THE URINARY ORGANS, 611 

or colloid material, the result of degeneration of the epithelial lining 
of the cyst. Sometimes very large cysts of this character are met 
with in cases of nephritis, or even in otherwise healthy kidneys (Fig. 
285). Cysts observed in kidneys which show no other disease 




Fig. 285.— Large retention-cyst of kidney (from a specimen in the Museum of the Phila- 
delphia Hospital). 

are probably due to undiscovered obstructions of the uriniferous 
tubules. 

Congenital cystic kidneys are of striking appearance. Usually 
both kidneys are affected, and are transformed into masses com- 
posed of innumerable cysts varying in size from microscopic points 
to cavities as large as a walnut (Fig. 286). On section the cysts 
are found to be filled with clear urinous liquid, or with colloid 
material, and between them is a stroma of more or less firm 



612 TEXT-BOOK OF PATHOLOGY. 

fibrous tissue. The pelvis of the kidney is usually preserved. 
These cysts are formed by dilatation of the uriniferous tubules 
and Malpighian bodies, probably as the result of some fetal disease 




Fig. 286— Congenital cystic kidney (Specimen 2816, Museum N. Y. Hosp.).' 

which causes obstruction of the tubules at their outlet at the apex 
of the pyramids, or in consequence of faulty union between the upper 
and the lower segments of the uriniferous tubules in the develop- 
ment of the organ. Similar cystic degeneration, with enlargement 
of one or both kidneys, may occur in later life. Finally, cystic 
adenoma may again be alluded to. 

PARASITES. 

Bacteria occur in the kidney in various affections : thus 
pneumococci, typhoid bacilli, the bacilli of glanders and anthrax, 



DISEASES OF THE URINARY ORGANS. 



613 



have been repeatedly demonstrated. In pyelonephritis the Bacil- 
lus coli communis is probably the usual active etiologic agent. 
Streptococci occur in the nephritis of septic conditions and 
in primary infectious nephritis of cryptogenic origin. Bacte- 
ria are occasionally found in the uriniferous tubules without 
gross lesions of the kidney, and are probably excreted with the 
urine. 

Streptococci occur in the urine in the nephritis of septic con- 
ditions, and in primary infectious nephritis of cryptogenic origin. 
Various other bacteria may be met with in the urine (see Bac- 
teriuria). 

Animal parasites are occasionally observed, such as echino- 
coccus-cysts, filarise, the eggs of Distoma hematobium, amcebse, 
and infusoria. Round worms and the oxyuris sometimes migrate 
into the bladder or enter through fistulse. 

The echinococcus-cyst occurs in the form of hydatids, which 
may perforate into the pelvis of the kidney and discharge with 
the urine, or become inspissated and calcify. The Cysticercus 
cellulosse and Pentastomum denticulatum are extremely rare. 
The Filaria sanguinis hominis occurs in the lymphatic spaces and 
in the blood-vessels of the kidney in cases of filariasis with chyl- 
uria. The kidneys in these cases show a waxy appearance on 
section, especially toward the apices of the pyramids, and the 
surface of the kidney may be abnormally lobulated. Microscopi- 
cally the lymphatic spaces about the uriniferous tubules are greatly 
distended. 

The Distoma hematobium occasionally produces pyelitis and 
pyelonephritis, with enlargement of the pelvis of the kidney. 

THE PELVIS OF THE KIDNEY AND URETER. 

CONGENITAL AND ACQUIRED MALFORMATIONS. 

Occasionally the pelvis or ureters, or both, may be absent or 
imperfectly developed. Complete obliteration of the ureter may 
be observed. More frequently there are two pelves or ureters, 
and when this is the case the malformation is, as a rule, bilateral. 

Obstructions of the ureter may be due to twists, to con- 
genital atresia, or to other diseases of the ureter, particularly at 
its entrance into the bladder. It may be brought about by the 
lodgement of renal calculi, by tumors of the ureter, or by pressure 
upon it from without. The outflow of the urine may be obstructed 
by diseases of the bladder, and particularly by stricture of the 
ureter. 

Dilatation of the ureter results from the conditions just 
named, and may reach considerable dimensions (Fig. 287). When 



614 



TEXT-BOOK OF PATHOLOGY. 



the obstruction is continued the dilatation may affect the pelvis 
of the kidney as well, and eventually the latter may be enor- 
mously enlarged. The pyramids become 
flattened, and the renal substance may 
undergo progressive atrophy, so that the 
kidney is converted into a sac-like for- 
mation filled with clear liquid, partly 
urine secreted in the earlier stages and 
partly transudate formed after the com- 
pression has stopped the renal function. 
To this condition the term hydronephro- 
sis is applied. 

CALCULUS. 

Calculi are of frequent occurrence 
in the pelvis of the kidney, and are 
formed by the precipitation of various 
normal or abnormal constituents of the 
urine. There may be merely small 
gritty particles lying in the calices or in 
the pelvis, to which the term renal sand, 
or gravel, is given ; or there may be 
large stones, almost filling the pelvis 
and calices, and forming more or less 
no. 287.-Diiatation of the accurate moulds of these. The most fre- 

ureter due to calculous obstruc- ■ « , , „ 

tion. quent iorms are those composed 01 uric 

acid and oxalate of lime, but phosphate 
and carbonate of calcium and triple phosphate calculi are occa- 
sionally found. Stones composed of cystin and xanthin are rare. 
Uric-acid calculi are composed of the acid itself, or of urates, and 
present themselves as yellowish, brownish, or red, smooth or some- 
what irregular formations. Those composed of oxalate of lime 
are irregular in shape and of brownish or red color. 

The results of renal calculi may be trivial or serious. Small 
particles of renal sand are frequently passed without serious dis- 
turbance. Large calculi tend to set up inflammation of the pelvis 
of the kidney, and may obstruct the outflow of the urine, causing 
hydronephrosis (Fig. 288). In some cases cancer seems dependent 
upon the continued irritation of a retained calculus. 

INFLAMMATION. 

Inflammation of the pelvis, or pyelitis, may result from 
the irritation of poisons ingested, such as cantharides, turpentine, 
and the like, or it may occur in the course of infectious diseases of 
various kinds. More frequently it results from the irritation of a 
calculus, or from ascending inflammation consequent upon cystitis 




DISEASES OF THE URINARY ORGANS. 



615 



and ureteritis. The mucous membrane becomes reddened and 
swollen, and not rarely is marked with hemorrhagic ecchymoses. 
The surface is covered with more or less desquamated epithelium 
and pus-cells. The inflammation may extend to the substance of 
the kidney {pyelonephritis). Considerable purulent exudate may 
take place, particularly when there is a calculus partially obstruct- 
ing the ureter. When there is complete obstruction the pelvis may 
become dilated with pus, and the calices or the entire kidney may 
be converted into a large pus-sac (pyonephrosis). Deposits of tri- 
ple phosphate may occur in pyelitis, and may occasion incrusta- 
tions upon the mucous surface. 

Inflammation of the ureter, or ureteritis, may occur 
under the same conditions as pyelitis. The mucous membrane 
of the ureter becomes swollen and reddened, as in catarrhal in- 
flammations elsewhere, and 
there may be erosions or 
superficial ulcerations. The 

other coats are thickened i!S\2K&^K' 
by inflammatory infiltration /" 
and, in chronic cases, by 
fibrous-tissue overgrowth. £ * 





Fig. 288— Calculus in the pelvis 
of the kidney and upper part of 
the ureter. 



Fig. 289.— Tuberculous pyelonephritis (modified 
from Bollinger). 



INFECTIOUS DISEASES. 



Tuberculosis of the pelvis of the kidney may occur as a 
miliary tuberculosis, or in the form of caseous nodules or masses. 
The latter may be primary and hematogenous in origin, or may 



616 



TEXT-BOOK OF PATHOLOGY. 



result from ascending infection (Fig. 289). In such instances 
the mucosa becomes more or less extensively infiltrated, and later 
caseous and ulcerated. The process extends to the calices, and 
subsequently to the pyramids and other parts of the substance of 
the kidneys. The pelvis may contain considerable quantities of 
caseous or puriform matter, and the kidney-substance may be 
extensively involved. The urine contains pus-corpuscles and 
often tubercle bacilli in great numbers. Tuberculosis of the 
ureters leads to nodular or diffuse thickening, and commonly to 
more or less obstruction (Fig. 290). 




Fig. 290.— Tuberculous nodule in the wall of the ureter, with beginning hydronephrosis 
(from a specimen in the Museum of the Philadelphia Hospital). 

TUMORS. 

Primary cancer is extremely rare. Secondary cancer may affect 
the pelvis in association with the kidney, or the ureters in asso- 
ciation with the bladder. Small cystic formations are not uncom- 
monly seen in the mucous membranes of the ureters, and may be 
due to inflammatory obstruction of the crypts, to proliferation 
and softening of the lymphoid follicles, or to parasitic invasion 
(psoi'ospermice). 

PARASITES. 

Round worms have occasionally been found in the ureters. 
The eggs of Distomum haematobium are frequently deposited in 
the mucous membrane, and occasion inflammation and papillom- 
atous excrescences. 



DISEASES OF THE URINARY ORGANS. 



617 



THE URINARY BLADDER. 

MALFORMATIONS. 

Congenital malformations of the bladder are compara- 
tively common. Among the more important is exstrophy. The 
anterior wall of the abdomen and of the bladder being wanting, 
the mucous membrane, with the openings of the ureters, is ex- 
posed to view. Not uncommonly this condition is associated 
with epispadias, or division of the clitoris. Sometimes the small 
intestine discharges through the exstrophic bladder, the large in- 
testine being contracted or completely absent. 

Occasionally the urachus remains patulous in consequence of 
atresia of the neck of the bladder or urethra, and the urine is dis- 
charged from the umbilical end. In other cases the urachus is 
closed at either end and the intervening portion is dilated, with 
the formation of a cyst. Again, there may be only partial oblit- 
eration of the urachus, the remaining portion in connection with 
the bladder being patulous and greatly dilated, forming a congenital 
adventitious sac. In one case under my observation this consti- 
tuted a cavity of considerable size, and when filled distended the 
abdomen as far as the umbilicus. Congenital diverticula may 
occur in the anterior wall, and less commonly at the sides of the 
bladder. Complete absence of the bladder, division into lateral 
portions by a septum (vesica bipartitis), and other congenital 
defects are rare. 

Acquired Malformations. — Dilatation of the bladder may 
result from congenital or acquired stenosis of its neck, or of the 
urethra ; or from paralysis of its walls, in consequence of disease 
of the spinal cord or nerves. The organ may be greatly increased 
in size, often reaching the umbilicus. When the dilatation is 
acute the walls are greatly thinned, but when it has been gradu- 
ally developed compensatory hypertrophy of the muscularis and 
of the submucous fibrous tissues leads to thickening of the walls. 
In these cases the mucous surface presents a ribbed appearance, 
fibrous-tissue bands standing out prominently and the mucosa 
being pouched between the bands. Diverticula of considerable 
size may form in this way, and the walls of the bladder sometimes 
present a considerable number of pouches. 

CHANGES OF POSITION. 

The position of the bladder, or of portions of it, is sometimes 
abnormal. Thus it may enter into a hernia, or a part of the wall 
of the bladder may prolapse with the wall of the vagina, forming 
vaginal cystocele. The latter is due to the traction of the pro- 
lapsing uterus, or to repeated overdistention of the bladder, with 



618 



TEXT-BOOK OF PATHOLOGY. 



weakness of the anterior vaginal wall. Complete inversion of 
the bladder through the urethra is occasionally observed in 
women. 

RUPTURE. 

Rupture of the bladder may be due to traumatism, and particu- 
larly to perforation by fractured pelvic bones. Rupture from 
overdistention is rare. Occasionally it may result from abdominal 
compression when the bladder is distended with urine, and ulcera- 
tive processes beginning in the mucous membrane may perforate 
the wall, or phlegmonous inflammations or degenerating new- 
growths surrounding the bladder may lead to perforation. In 
women perforations are frequently established between the blad- 
der and vagina in consequence of pressure of the fetal head or of 
forceps, and vesicovaginal fistula results. Perforation into the 
peritoneal cavity is usually followed by fatal acute peritonitis. 
Rupture into the tissues below the peritoneal reflections gives 
rise to widespread infiltration of urine and phlegmonous or gan- 
grenous inflammation. 

CIRCULATORY DISTURBANCES. 

Active hyperemia may result from irritant poisons, such as 
cantharides, or may occur in persons suffering from paraplegia, in 
consequence of disturbances of innervation. 

Passive hyperemia occurs when there is pressure upon the 
inferior vena cava or thrombosis of that vein. The mucous mem- 
brane becomes dark-red and is often marked with punctate hem- 
orrhages. Considerable varicosity of the veins at the neck of the 
organ may occur, and may give rise to copious hemorrhages, or to 
obstruction and retention of the urine. 

Hemorrhages in the mucous membrane occur in severe con- 
gestion or inflammation, and in various hemorrhagic diseases. 
Large hemorrhages into the cavity itself may result from trauma- 
tism from without, or from calculi. The varicosities before men- 
tioned may occasion considerable hemorrhage, as may also papil- 
lomatous or other new-growths. Large quantities of blood with 
little admixture of urine may lead to the formation of dense clots 
within the organ, but when the quantity is small the blood is 
mingled with the urine. 

INFLAMMATION. 

Inflammation of the bladder, or cystitis, varies in ex- 
tent, duration, and character. Acute cystitis may result from irri- 
tant poisons excreted with the urine, and frequently attends acute 
infectious diseases. In these cases, however, the disease is gener- 



DISEASES OF THE URINARY ORGANS. 



619 



ally mild. More intense forms occur from extension of inflamma- 
tion to the bladder in cases of urethritis, or when septic material 
is introduced in catheterization. Retention and decomposition of 
the urine from strictures or prostatic hypertrophy are frequent 
causes of chronic cystitis. 

Cystitis may present itself as a mucopurulent catarrh, acute or 
chronic in course ; as phlegmonous inflammation ; or as a pseudo- 
membranous process. 

Mucopurulent cystitis in the acute stages causes swelling of the 
mucous membrane, with injection of blood-vessels and sometimes 
punctate hemorrhages. The surface, especially at the base, is 
covered with mucopurulent exudate of a tenacious character, in 
which pus-cells and desquamated epithelium are abundant. The 
urine tends to undergo ammoniacal fermentation. 

In chronic cases thickening of the submucosa and hypertro- 
phy of the muscularis cause great thickening of the organ, and 
the surface within is usually ribbed from the prominence of the 
fibrous-tissue bands and the pouching of the mucous membrane 
between the bands (Fig. 291). Erosions and ulceration may oc- 




Fig. 291— Dilated ribbed bladder. 



cur upon the surface, and occasionally perforation of the walls 
takes place. Incrustations of triple phosphate and of other 
common salts frequently cover the surface. 

Phlegmonous cystitis results from intense infections, or from the 
retention of urine in paraplegia. The submucous tissue is consid- 
erably swollen and infiltrated, and complete perforation of the 
walls and paracystitis or phlegmonous inflammation of the tissues 
surrounding the bladder may ensue. 



620 



TEXT-BOOK OF PATHOLOGY. 



Pseudomembranous cystitis occurs in certain severe infectious 
diseases, and may present itself in the form of a typical pseudo- 
membrane, or as a combination of phlegmonous and pseudomem- 
branous inflammation. Occasionally pseudomembranes are formed 
without any inflammatory process, in nervous individuals, and in 
the course of or after pneumonia I have seen a cast of the entire 
bladder of this nature. 

INFECTIOUS DISEASES. 

Tuberculosis of the bladder is usually secondary to tubercu- 
losis of the kidney, or to that of the prostate, seminal vesicles, or 
epididymis. Tubercular ulcers independent of tuberculosis else- 
where in the urogenital tract may occur in phthisis or intestinal 




Fig. 292.— Tuberculosis of the bladder (Orth). 



tuberculosis, but such cases are rare. The lesions observed in 
tuberculosis of the bladder are ulcerations, for the most part occu- 
pying the base and surrounding the orifices of the ureters, and 
there may be distinct or clustered tubercles. Numerous small 
ulcers, or a single large ulcerated surface may be observed (Fig. 
292). Deposits of triple phosphate frequently form incrustations 
on the surface. 

Syphilitic ulcers have been observed in the bladder, but are 
extremely rare. 



DISEASES OF THE URINARY ORGANS. 



621 



CALCULI AND FOREIGN BODIES. 

The bladder is the commonest seat of urinary calculi. They 
may occur in the form of fine particles or gravel, or as stones of 
considerable size. Usually there is but one ; sometimes a consid- 
erable number may be present. The shape and general appear- 
ance depend upon the composition of the stone. 

The formation of calculi is due to precipitation from the urine 
of its various earthy or other constituents as the result of stagna- 
tion and fermentative change. Foreign bodies often form the 
nuclei of stones, and thus a calculus in the bladder may form 
around broken portions of catheters, hairpins, or other foreign 
bodies inserted into the urethra. Similarly, parasites may be the 
nucleus, and in ordinary cases of stone the mucous or degenerated 
epithelial cells constitute the focus about which the deposit occurs. 
There is practically never a simple sediment of saline or earthy 
material, but a combination of the latter with some albuminous 
matrix. Catarrhal conditions of the bladder, especially when 
combined with stagnation of the urine as the result of hypertrophy 
of the prostate, urethral stricture, and the like, are the most com- 
mon antecedent causes. 

Calculi in the bladder may be composed of uric acid or urates, 
of oxalate of lime, of various phosphates, of carbonate of lime, or 
of certain organic compounds. 

Uric acid and urate calculi are less common in the bladder 
than in the kidney. They result from surcharge of the urine 
with uric acid in lithemic or gouty individuals, and from acid 
decomposition rendering the uric acid and urates insoluble. They 
are yellowish or red in color, rounded, slightly granular or smooth 
upon the surface, and, as a rule, quite hard. The calculi com- 
posed of urates are usually more irregular and softer, and are 
generally lighter in color. Frequently phosphates are combined 
with them. 

Phosphatic calculi may be of several kinds ; they may be com- 
posed of phosphate of lime, triple phosphate, or mixed phosphates. 
They form the most frequent variety of calculi and concretions in 
the bladder, and are generally due to alkaline decomposition 
causing a deposit of the simple phosphate of lime or of the 
combination of phosphate of magnesium with ammonium phos- 
phate, known as triple phosphate. These deposits may occur in 
the form of incrustations upon the surface of the bladder in 
various diseases, or in the form of irregular, soft, and more or 
less white calculi. 

Oxalate of lime occasions rounded, hard calculi, of brownish 
color and of irregular, granular surface, from which they derive 
the name mulberry calculi. They occur in conditions similar to 
those causing uric-acid stones. 



622 



TEXT-BOOK OF PATHOLOGY. 



Calculi composed of carbonate of calcium, sulphate of calcium, 
cystin, xanthin, and indigo are extremely rare. 

Results of Urinary Calculi. — While cystitis and retention 
of urine frequently cause stone, the latter is prone to occasion in- 
creased irritation and inflammation, and may cause serious obstruc- 
tion to the outflow of urine, and thus retention in the bladder. 
Ulceration may take place, and perforation of the bladder- walls 
may ensue. Hypertrophy of the walls occurs when the stone only 
partially obstructs the outflow, and under the same conditions the 
ureters may become distended and hydronephrosis may occur. 




Fig. 293.— Tuft of papilloma of the bladder (thionin ; X 90) (Martin and Taylor). 

Not rarely the stone lies in a pouched dilatation of the wall of 
the bladder, either from having been formed in that situation in 
consequence of stagnation of the urine, or from having caused a 
dilatation by weakening the walls at a certain point. Complete 
encapsulation of the stone has been observed in such cases. 

TUMORS. 

Polypoid outgrowths from the mucosa may be observed in 
chronic cystitis. 

Papillomata occur either as the result of chronic irritation, 



DISEASES OF THE URINARY ORGANS. 



623 



or as apparently causeless tumors. The papilloma presents itself 
as a somewhat cauliflower-like elevation affecting the base, and 
sometimes considerable portions of the mucosa, and has a whitish 
or grayish color. It is usually vascular, and therefore frequently 
occasions hemorrhages. 

Microscopically it is composed of a delicate connective-tissue 
stroma containing large, thin- walled blood-vessels, and covered 
with cylindrical epithelium (Fig. 293). Occasionally papillomata 
become transformed into malignant epitheliomatous growths. 

Carcinoma is a rare form of primary tumor. It occurs as a 
somewhat papillomatous thickening of the mucosa, or as a more 
considerable infiltration of the wall of the bladder (Fig. 294). 




Fig. 294. — A, epitheliomatous tumor ; B, wart-like growths ; C, villous growths (Clado). 

Microscopically it is composed of large polymorphous epithelial 
cells infiltrating the walls more or less deeply and irregularly, or 
arranged in acini or alveolar formations. 

Secondary carcinoma of the bladder may result from ex- 
tension of prostatic or uterine cancer. Very rarely the bladder is 
involved by metastasis. 

Fibroma, fibro-adenoma, myoma, and myxoma are occa- 



624 



TEXT-BOOK OF PATHOLOGY. 



sionally observed, and cysts may be formed by closure of pouched 
diverticuli or by distention of the patulous urachus. Cysts of 
obscure origin are sometimes met with ; dermoid cysts are rare. 
Sarcoma is very rare. 

ABNORMAL CONDITIONS OF THE URINE. 

Quantity. — The normal quantity in the adult is from 1500 to 
2000 cc. Conditions which check the perspiration or action of 
the bowels increase the amount of urine ; excessive sweating and 
diarrhea have the reverse effect. In the latter case the excretion 
may be almost suppressed {anuria). The same may occur in acute 
nephritis, or chronic nephritis with uremia, in extreme anemia, 
and in acute or chronic obstructive conditions in the gastro-intes- 
tinal tract interfering with absorption of water. Occasionally 
anuria is reflex, resulting from obstruction of the urinary passages 
by calculi. The quantity of urine is increased {polyuria) in cases 
of excessive consumption of water, and habitually in diabetes 
mellitus and insipidus and in chronic interstitial nephritis. 

Specific Gravity. — Normally the specific gravity is 1015 to 
1020. It becomes increased when the amount of urine is de- 
creased, and vice versa. The specific gravity is especially high in 
diabetes mellitus, despite the polyuria, sometimes reaching 1040 
or 1050. It is low in most forms of chronic nephritis, in diabetes 
insipidus or simple polyuria, and in anemia and hysteria, or other 
nervous diseases. 

Color. — The normal amber color is due to the presence of 
various pigments, especially urobilin and uroerythrin. These are 
derivatives of hemoglobin or bilirubin. 

In pathologic conditions other pigments, such as hematopor- 
phyrin, pathologic urobilin, melanin, etc., are met with. Indicah 
is present in the urine in the form of a chromogen, which may 
sometimes become oxidized, with the formation of dark-colored 
pigment-animal indigo. Certain drugs eliminated with the urine 
cause discolorations. Bilirubin occurs in jaundice and other con- 
ditions, and blood or hemoglobin may cause discoloration. 

Reaction. — The normal reaction is acid, but frequently after 
meals it becomes neutral or even alkaline. The ingestion of cer- 
tain foods rich in alkalies or acids, which become converted into 
alkaline carbonates (citrates, acetates, etc.), may occasion an alka- 
line reaction, while other acids lead to the opposite result. De- 
composition of the urine usually causes an intense alkaline reaction, 
by conversion of the urea into ammonia. Occasionally the reac- 
tion of the urine is amphoteric, both red and blue litmus-paper 
being acted upon. 

Glycosuria is a term applied to the presence of glucose or 
grape-sugar in the urine. This may be a transient condition in 



DISEASES OF THE V BINARY ORGANS. 



625 



various diseases, such as chorea, cerebrospinal fever, whooping- 
cough, and epilepsy, and is not uncommon in gouty persons 
indulging in a free diet. Sometimes it results from the effects 
of poisons, such as morphin, chloroform, or carbonic oxid ; but 
in some of these cases the reactions of glucose are simulated 
by other and quite different reducing-substances present in the 
urine. Permanent and decided glycosuria is characteristic of dia- 
betes mellitus only. 

Iyevulosuria, the presence of fruit-sugar, lactosuria, that 
of milk-sugar, and dextrinuria, that of dextrin in the urine, 
have been discovered. 

Choluria is the name indicating the presence of biliary pig- 
ments and acids in the urine. It is most frequently observed 
in cases of jaundice due to hepatic disease, but may also occur in 
so-called hematogenous jaundice, the formation of the pigment in 
some of the latter cases probably taking place in the kidneys them- 
selves. The urine presents a dark color, varying from brownish 
to greenish. Oxidizing substances, such as fuming nitric acid, 
produce a play of colors. 

Microscopically the cellular constituents of the urine are found 
stained, and granular concretions of bilirubin or rhombic crystals 
may be observed. Hyaline casts, more or less deeply stained by 
the pigment, are frequently seen. 

XJrobilinuria. — Urobilin occurs in the normal urine mainly as 
a chromogen, or is converted into urobilin on the addition of acid. 
Sometimes, urobilin is present in large quantities in the fresh urine. 
This has been particularly observed in fevers, in jaundice, and in 
certain anemic diseases, especially in pernicious anemia. 

Indicanuria. — Indigo-blue occurs in the urine as a chromo- 
gen which gives rise to the formation of indigo on decomposition. 
This indican, or indoxyl sulphate, is a product of indol derived 
from the intestine, and an excess of indican in the urine is sig- 
nificant of intestinal decomposition. 

Other forms of the ether-sulphuric acid series occur in the 
urine, but are less significant. 

Acetonuria occurs to a slight extent in health, but more par- 
ticularly in conditions of inanition, in gastro-intestinal disturbances, 
and in fever. It is especially significant in diabetes mellitus, and 
may become very pronounced toward the latter end of this affec- 
tion. 

Diaceturia, or the condition in which diacetic acid appears in 
the urine, is also met with in fevers and inanition, but particularly 
in diabetes. 

I/ipaciduria refers to the presence of fatty acids in the urine, 
but has no special significance. 

Hydrothionuria refers to the presence of sulphuretted hydro- 
gen in the urine. This is noted occasionally in autointoxications, 

40 



626 



TEXT-BOOK OF PATHOLOGY. 



or as the result of fermentative changes in the urine. The urine 
may have a foamy appearance, to which the term pneumaturia is 
sometimes applied. Other gases may be present, but only in 
small proportion and rarely. 

Melanuria is a term applied to the dark discoloration of the 
urine occasionally seen in persons suffering from pigmented tumors. 
It also occurs in phthisis and other wasting diseases. As a rule, the 
urine becomes darker after addition of oxidizing substances, but it 
may be quite dark when passed. It contains iron and sulphur. 

Albuminuria. — Minute traces of serum-albumin probably 
occur in the normal urine. The term albuminuria, however, is 
applied to cases in which albumin is readily detected. It may be 
accidental — that is, dependent upon the admixture of albuminous 
substances from the mucous membrane lining the urinary passages, 
— or essentially renal in character. In the former instances the 
presence of abundant blood or pus-cells indicates the nature of the 
case. True renal albuminuria consists of the excretion with the 
urine of serum-albumin and serum-globulin, the former being con- 
siderably more abundant than the latter. Pure serumuria is ex- 
tremely rare, and pure globulinuria perhaps even more so. 

Albuminuria is more frequently the product of actual renal dis- 
ease or nephritis, and is then due to the disease of the epithelium 
of the glomeruli and tubules. A certain amount of albumin occurs 
in degenerative or congested conditions of the kidneys ; in various 
general diseases affecting the blood without manifest disease 
of the kidney, such as anemias, diabetes, and the like ; in certain 
nervous affections probably influencing the circulation ; and in dis- 



At times albuminuria is periodic or cyclic, this periodicity 
depending upon general conditions, such as diet, exposure, and exer- 
cise, which in turn affect the blood or renal circulation. Consid- 
erable amounts of albumin in the urine are never physiologic. 

Large proportions of globulin occur in amyloid disease of the 
kidneys. 

Albumosuria. — Various albuminous substances derived from 
serum-albumin or serum-globulin, and not coagulable by heat, 
occur in the urine. These are hydration-products designated 
albumoses or propepton. True pepton has never been found in 
the urine. Albumosuria occurs in cases in which pus-cells or 
large exudates are undergoing absorption, as in septic processes, 
pneumonia, and the like (pyogenic albumosuria). In another 
group of cases intestinal malassimilation or decomposition comes 
into play (enter ogenic albumosuria). In the third group diseases 
of the blood, such as leukemia and various intoxications, are 



orders of the digestive tract. 




DISEASES OF THE URINARY ORGANS. 



627 



Nucleo-albtiminuria. — Nucleo-albumin, formerly supposed 
to be mucin, is derived from the protoplasm of the surface-epithe- 
lium of the urinary tract, and occurs in the urine in small quantity 
in nearly all persons, and in large quantity when there is irritation 
of the lining mucosa, particularly in pyelitis and cystitis. 

Fibrinuria occurs in conditions in which lymph or blood gains 
access to the urinary passages. Fibrinous casts or shreds may be 
.passed, or small flocculent particles are observed. Fibrinuria is 
usually associated with hematuria or chyluria. 

Hematuria is a term applied to the presence of blood in the 
urine. This may be accidental from admixture of menstrual 
blood and the like, or may be a pathologic condition, in which the 
blood originates from the kidneys, ureters, bladder, urethra, or 
other parts of the urinary system. Renal hematuria may result 
from intense congestion or from hemorrhagic nephritis. Trauma- 
tism, either from without or from calculi in the pelvis, is a fre- 
quent cause. Tumors and specific inflammatory processes are occa- 
sional causes. Sometimes hematuria is due to intense anemia, 
hemorrhagic diseases, or severe intoxications. Hematuria which 
is due to admixture of blood with the urine below the kidney 
results from traumatism, injury by calculi or catheterization, from 
vascular tumors, and occasionally from inflammatory or other dis- 
ease-processes. 

Renal hematuria is distinguished from that originating in the 
bladder by the intimate admixture of urine and blood, and by the 
associated evidences of renal disease — renal epithelium, tube-casts, 
etc. Fragmentation of the red corpuscles is said to indicate renal 
hematuria. In hematuria originating in the bladder larger clots 
may pass, in association with bladder-epithelium and mucin (nu- 
cleo-albumin). In cases of sudden renal hemorrhage large clots, 
sometimes forming casts of the pelvis, may be formed and dis- 
charged. 

Hemoglobinuria indicates the presence of free hemoglobin 
or of methemoglobin in the urine, without the presence of blood- 
corpuscles. Hemoglobinuria results from causes which lead to 
disorganization of blood and elimination of the coloring-matter 
through the kidneys. It is met with in various infectious dis- 
eases, such as malaria, and in intoxications, as in poisoning with 
potassium chlorate, carbolic acid, arsenic, and other drugs, or with 
toadstools. It occasionally results from snakebite or poisoning by 
other venomous animals. 

Paroxysmal hemoglobinuria is a form of intermittent disease 
especially frequent in subtropical countries. The attacks some- 
times seem to be determined by exposure to cold and other ex- 
ternal influences, whilst the predisposition may be dependent 
upon syphilis or other general disorders. The urine presents a 
dark-red or brownish color, and when tested with the spectro- 



628 



TEXT-BOOK OF PATHOLOGY. 



scope shows the bands indicative of hemoglobin or methemo- 
globin. 

Microscopically the hemoglobin may present itself in the form 
of granules or cast-like formations, or sometimes as crystals. 
Blood-corpuscles are absent, or at most present in extremely 
small numbers. 

I/ipuria. — A small amount of fat may appear in the urine in 

cases of advanced diffuse nephritis with fatty degeneration, and in 
certain cases of pyelitis. In other cases lipuria results from dis- 
orders in which there is excess of fat in the blood (lipemia). This 
occurs in cases of excessive consumption of oil or fatty food and 
in cases of intoxication, notably by arsenic. It is sometimes pres- 
ent in diabetes, phthisis, chronic alcoholism, and obesity, and fract- 
ures iujuring the marrow, or serious traumatism of the subcuta- 
neous fatty tissues may cause fat-embolism and lipuria. 

The appearance of the urine varies with the amount of fat, 
but, as a rule, there is a solid scum upon the surface, and there 
may be large oil-drops. Occasionally the urine is quite milky 
when recently passed. Microscopically, oil-drops are more or less 
abundant ; and fat-crystals may be discovered. 

Chyluria is the name applied to a milky condition of the 
urine which probably results from admixture of lymph or chyle. 
The urine is light colored, and more or less milky in appearance. 
Often there is a reddish discoloration from associated hematuria 
Qiematochyluria). The urine contains albumin and sometimes 
albumoses. 

Microscopically, numerous oil-drops of varying size and, usu- 
ally, blood-corpuscles are detected. The most frequent cause is 
the obstruction of the lymphatic channels and their subsequent 
rupture in the kidney or bladder in consequence of the lodgement 
of the Filaria sanguinis hominis. In these cases the embryos of the 
filarise are usually detected in the urine. Sometimes a chyluria is 
non-parasitic, but the causes are obscure. 

Bacteriuria. — Normally the urine contains no bacteria. In 
cases of cystitis or other inflammatory diseases, however, and par- 
ticularly when catheterization has been practised, bacteria of de- 
composition may be present, such as the Micrococcus urece, Bac- 
terium termo, the Barillas proteus, yeast-fungi, and other forms. 
Not rarely the Bacillus coli communis is met with, particularly in 
ascending infections of the urinary tract. In cases of certain in- 
fectious diseases, such as typhoid fever, pneumonia, and erysipelas, 
the specific micro-organisms may be found in the urine, having 
escaped from the blood through the capillaries of the glomeruli. 
Streptococci are also met with in primary and secondary infectious 
nephritis. The Bacillus tuberculosis may be discovered in cases 
of tuberculosis of the kidney, ureters, bladder, or other parts of 
the urinary tract (Fig. 295). It is frequently present in clusters, 



DISEASES OF THE URINARY ORGANS. 



629 



this constituting a marked point of distinction from the smegina- 
bacillus, which is often found in urine, especially that of women, 
and is easily mistaken for the tubercle-bacillus. Another point 




Fig. 295.— Tubercle bacilli in the urine ; from a case of tuberculous cystitis (Jakob). 

of distinction is the greater ease with which the smegma-bacillus, 
stained with carbol-fuchsin, may be decolorized by alcohol. Posi- 
tive differentiation in doubtful cases is made by injection of the 
urine into guinea-pigs. 

CHEMICAL CHANGES AND SEDIMENTS. 

The various inorganic and organic constituents of the urine 
may be present in excessive quantities, and may form deposits, or 
abnormal chemical substances may be detected. 

Uric acid is deposited in the form of yellowish, brownish, or 
reddish crystals of whetstone shape, or as irregular angular forma- 
tions superimposed or clustering together (Fig. 296). The color 
is due to uroerythrin, taken up from the urine. Excess of uric 
acid occurs in lithemic and gouty conditions, and the crystals may 
deposit from a highly acid urine, even though there be no excess. 

Oxalate Of lime occurs in the form of highly refracting octa- 
hedral corpuscles, their appearance being likened to that of an 
envelope (Fig. 297). Certain foods rich in oxalates may cause 
excessive excretion, and oxaluria occurs as an independent con- 
dition of obscure nature allied to gout and lithemia. Oxalates 
deposit from highly acid urine, even though no excess be present. 
This must be distinguished from oxaluria proper. 

Phosphates. — Various forms of phosphates are found in 
crystalline form in urinary sediments. Basic phosphate of mag- 
nesium and neutral phosphate of lime are found in urine becoming 
alkaline, while the phosphate of ammonium and magnesium, or 



630 



TEXT-BOOK OF PATHOLOGY. 



triple phosphate, is met with when alkaline decomposition takes 
place. It presents itself in different forms, the most characteristic 
being the large coffin-lid crystals and certain star-shaped forma- 
tions (Fig. 298). Triple phosphate is especially abundant in 
cystitis with alkaline decomposition of the urine in the bladder. 




Fig. 296.— Various forms of uric-acid 
crystals. 



Fig. 297.— Various forms of crystals of 
oxalate of calcium. 



Urates. — Urates are deposited from acid urines as a whitish 
or reddish sediment of amorphous character. The reddish color 
sometimes observed is due to admixture of urinary pigment. In 
decomposing urine, of somewhat alkaline reaction, urate of ammo- 
nium is deposited as hedgehog crystals or masses (Fig. 299). 




Fig. 298.— Crystals of triple phosphate 
(ammonium-magnesium phosphate). 





pr vf <^> 



Fig. 299. — Urate of ammonium crystals. 



HippuriC acid is rarely met with, excepting after the inges- 
tion of benzoic acid or of certain fruits. It forms long, prismatic 
crystals, which occur in groups. 



DISEASES OF THE URINARY ORGANS. 



(331 



Carbonates and sulphates are rarely observed in urinary 
sediments. 

Fat- crystals occur in the form of fine needles, or of aggre- 
gations arranged in a star-like manner and resembling tyrosin 
groups (Fig. 300). They are found in cases of chronic nephritis, 
pyelitis, and cystitis. 

Tyrosin. — This substance usually occurs in the urine in solu- 
tion, or rarely in the form of sheaves composed of fine needles 
arranged in star-like clusters (Fig. 300). 

I/eucin occurs as small spheres, often having a sorue , vdiat 
radiated structure within. These are most readily discovered 
when the urine has been partially evaporated. 

Leucin and tyrosin are observed in acute yellow atrophy of the 




Fig. 300.— Leucin-spheres and tyrosin- Fig. 301— Cholesterin-plates and fat-crystals 
needles. (needles). 



liver, in phosphorus-poisoning, and occasionally in severe infec- 
tious fevers. 

Cystin occurs in the form of hexagonal plates often super- 
imposed. They are most frequently associated with cystin calculi 
in the kidney, 

Xanthin is extremely rare, but may be associated with xan- 
thin calculus. 

Cholesterin appears in the form of flat, quadrilateral plates, 
with a re-entering angle at one of the corners (Fig. 301). They 
are met with in old cystitis or pyelitis, but are rare. 

Indigo. — Amorphous particles or crystals of indigo may be 
found in urine containing great excess of indoxyl sulphate. They 
present a characteristic bluish color. 

Bilirubin, hemoglobin, methemoglobin, and hema- 
toidin are occasionally seen as brownish granular concretions or 
in the form of rhombic crystals (see Choluria, Hemoglobin- 
uria). 



632 



TEXT-BOOK OF PATHOLOGY. 



THE URETHRA. 

CONGENITAL ABNORMALITIES. 

Absence of the urethra is sometimes met with in association 
with other defects of development. Partial deficiencies and ab- 
normal structure of the urethra are more frequent. Thus in the 
female it may be reduced in length and open in the anterior w T all 
of the vagina, and in the male may terminate at the base of the 
scrotum. Obliteration of part of the urethra (atresia) may occur 
in cases of defective development of the corpus spongiosum ; more 
commonly there is obliteration of the meatus. Other abnormal 
conditions will be considered in connection with defective develop- 
ment of the penis. 

INFLAMMATIONS. 

Inflammation of the urethra, or urethritis, is most fre- 
quently due to a specific micro-organism — the gonococcus of 
Neisser. Some cases, however, are non-specific, resulting from 
irritation by chemical or mechanical agents with associated infec- 
tion (staphylococci, streptococci, or other organisms). Some of 
these cases are caused by direct traumatism, as by blows, injuries 
caused by catheterization, and the like ; in other cases foreign 
bodies, as calculi, become lodged in the urethra and occasion in- 
flammation, or injure the urethra in passing. Urethritis, like in- 
flammations of other mucous membranes, may occur in various 
infectious diseases, such as typhoid fever, scarlet fever, small-pox, 
etc. In the female, inflammations of the vagina and vulva fre- 
quently extend to the urethra. A form of pseudomembranous 
urethritis of obscure origin has been observed in a few cases. 

Specific urethritis, or gonorrhea, is always due to direct infec- 
tion with the gonococcus (for description of the organism, see 
Part I.). Certain conditions of the urethra favor infection ; thus 
an adherent prepuce, by causing greater retention of the infective 
matters, increases the liability, and probably congested and irri- 
tated states of the urethral mucosa heighten the susceptibility. 
The vulnerability of different individuals probably varies ; and 
doubtless the micro-organism has greater virulence in some in- 
stances than in others. 

Pathologic Anatomy. — Urethritis usually first affects the mucosa 
at or near the meatus, but tends to spread rapidly to the posterior 
parts. The mucosa is at first intensely congested, red, and swollen. 
Soon a purulent exudate, of yellowish or greenish color, makes its 
appearance. The small crypts or lacunae swell and become dis- 
tended with purulent exudate. 

Microscopically, urethritis presents the features of an intense 
purulent catarrh. Within a few days of the onset the super- 
ficial epithelium becomes loosened and begins to desquamate ; 



DISEASES OF THE URINARY ORGANS. 633 

and at the same time polymorphonuclear leukocytes make their 
way to the surface between the epithelial cells. The pus-cells 
and epithelium of the surface-exudate contain gonococci in abun- 
dance, and the organisms are discovered in the cells and to a less 
extent between the cells of the deeper layers of the mucosa (Fig. 
302). The process extends most deeply in those parts of the 




Fig. 302.— Acute urethritis, showing purulent infiltration and gonococci in the cells and 
between the cells (Birch-Hirschfeld). 

urethra (penile portion) in which the lining epithelium is of the 
columnar variety. 

Associated Lesions. — In simple cases the disease proceeds no 
further than has been described, but after a period of several 
weeks gradually subsides. Very frequently, however, the inflam- 
mation extends in various directions, and complicating conditions 
arise. Sometimes the infective agents penetrate the membrana 
propria of the small glands (Littre's glands), or enter the sub- 
mucosa by direct invasion through the interglandular parts of the 
mucosa. Leukocytic collections in the submucosa or periurethral 
abscesses may result. In these cases the gonococcus alone may be 
the infective cause, or other pyogenic organisms may be associated ; 
sometimes periurethral lesions are caused by staphylococci inde- 
pendently of gonococci. Occasionally accumulations of pus in 
Tyson's glands may simulate periurethral abscesses. In the fe- 
male similar purulent distention of the glands of Bartholin is a 
frequent lesion. The inflammation of the urethra is often confined 
to the anterior portion (anterior urethritis), but may extend to the 



634 



TEXT-BOOK OF PATHOLOGY. 



posterior portion [posterior urethritis). In the male, secondary in- 
volvement of the prostate gland is likely to occur with posterior 
urethritis ; and, more rarely, the organisms invade the vas deferens 
and find their way to the epididymis, causing acute epididymitis. 
The bladder is rarely involved, the mucosa apparently offering 
considerable resistance to the infection. In the female, acute vag- 
initis, and especially inflammation of the cervix uteri, are com- 
monly associated. Secondary extension to the uterus may occa- 
sion gonorrheal endometritis ; more frequently the uterus is but 
little affected, while the Fallopian tubes suffer intense inflamma- 
tion. Catarrhal or purulent salpingitis, often complicated with 
local peritonitis, is one of the most important of the complications. 
When pus from a gonorrheal urethritis is brought in contact with 
the conjunctiva a severe form of purulent conjunctivitis results. 

Metastatic lesions are not infrequent. Among these, gonorrheal 
arthritis is the most familiar. It usually occurs late in the disease, 
sometimes after an interval of weeks or months from the onset, and 
involves the larger joints (knee, elbow, wrist). Purulent exuda- 
tion and fibrous anchylosis may result. A similar lesion is gonor- 
rheal tenosynovitis. Sometimes the pericardium, endocardium, and 
myocardium are involved ; and, more rarely, the pleura and the 
membranes of the cord. 

Enlargement of the lymphatic glands of the inguinal (bubo) 
region is frequent; sometimes it terminates in suppuration. 

Chronic urethritis is usually the result of continuation of the 
acute form. It may present itself in the form of a chronic catar- 
rhal process, as a hyperplastic inflammation, or as a productive or 
cicatrizing form. 

In the catarrhal form of chronic urethritis the lesion is practi- 
cally the same as in the acute disease. The epithelium is loosened 
and more or less desquamated, and sometimes distinct erosions are 
observed. Definite ulcerations may occur in parts back of strict- 
ures. The columnar epithelium may be converted into the squa- 
mous form in localized areas or diffusely. The crypts and glands 
of the mucosa may be distended with desquamated cells and 
more or less periglandular inflammation may be observed. 

In the hyperplastic variety the mucosa is thickened in a papil- 
lomatous manner, and diffuse catarrhal inflammation is associated. 

The productive or cicatrizing form is the most important. It 
*may be diffuse in character, but is usually localized and leads to 
stricture-formation. 

Stricture of the urethra is most frequent in the membranous 
portion, but may occur in the anterior parts. Not rarely there 
are several strictures in the course of the canal. Histologically 
the stricture is the result of productive inflammation of the mucosa 
and submucosa. It is therefore a lesion of slow development, and 
may not become obstructive for months or years after the acute 



DISEASES OF THE URINARY ORGANS. 



635 



attack of gonorrhea, to which it owes its origin, has subsided. 
The lumen of the urethra is encroached upon in limited area or 
for a considerable distance, and on section the stricture is found to 
be hard and resisting. When the lumen of the urethra is greatly 
narrowed the outflow of urine is impeded, and hypertrophy of the 
walls of the bladder results. Later, dilatation of the bladder, and 
even of the ureters and pelvis of the kidneys, may result. The 
urethra back of the stricture frequently presents the lesions of 
chronic catarrhal or hyperplastic urethritis, the obstruction serving 
to prolong the original inflammation of these parts. Rupture of 
the urethra and extravasation of urine into the cellular tissues, 
with subsequent necrosis and gangrene, may occur. 

In chronic urethritis there is usually a constant but slight dis- 
charge of mucous exudate (gleet). Examination of this may dis- 
cover no gonococci, or only an occasional group. The urine 
contains flocculent shreds (clap-threads), which on microscopic 
examination are found to be granular or homogeneous structures 
resembling cylindroids, and often covered with pus-cells that have 
adhered to the surface. The amount of discharge may be quite 
copious at times, especially in the hyperplastic and catarrhal forms 
of chronic urethritis. 

INJURIES OF THE URETHRA. 

The urethra may be injured by traumatism from without or 
within. In cases of falls with injury of the perineum the mem- 
branous portion of the urethra may be seriously lacerated, and in 
women injuries sustained during labor may cause immediate 
rupture of the urethra, or may first occasion inflammatory and 
necrotic changes in the anterior wall of the vagina and secondary 
perforation of the urethra. Injuries from within the urethra may 
be due to forced attempts at catheterization when some form of 
obstruction opposes the passage of the instrument. " False pas- 
sages " are thus occasioned, and may result in fistula? and extrava- 
sations of urine. Concretions or calculi from the kidney or bladder 
may lodge in the urethra, and may cause immediate perforation or 
primary inflammation, with secondary rupture of the walls. 

Rupture of the urethra causes extravasation of urine into the 
periurethral cellular tissues. If the skin is intact and the urine 
cannot escape, widespread inflammation, necrosis, and gangrene 
are liable to occur. Fistulous communications may be established 
with the exterior, or, in women, with the vagina. 

INFECTIOUS DISEASES. 

Gonorrheal urethritis is the important infectious disease 
of the urethra. For convenience, it has been described under 
Inflammations. 



636 



TEXT-BOOK OF PATHOLOGY. 



Tuberculosis of the vesical end of the urethra may be asso- 
ciated with tuberculosis of the bladder. Lupus sometimes in- 
volves the meatus and anterior end of the urethra in cases of lupus 
of the external genitalia of women. Very rarely tuberculosis of 
papillary form is met with in the urethral mucosa. 

Syphilis. — The chancre may occur in anterior parts of the 
urethra in either sex. It usually undergoes rapid ulceration. 

TUMORS. 

The urethra of women is more often the seat of tumors than is 
that of men. 

Small polypoid tumors are occasionally seen hanging from 
the meatus ; they may be of cystic character, like the polyps of 
other mucous membranes. 

Carcinoma is usually secondary to cancer of the external 
genitalia (vulva, vagina, glans penis). Primary carcinoma origi- 
nating from Cowper's gland has been described, and a few cases 
of carcinoma of other parts of the urethra have been observed. 

Cysts of the mucous membrane, due to retention of the con- 
tents of the small glands, are occasionally met with, especially in 
the posterior portion of the urethra. The inner lining of the cyst 
is elevated in the form of papillae covered with squamous epi- 
thelium. 

Sarcoma of the urethra has been described, but is very rare. 



CHAPTEE VIII. 
DISEASES OF THE REPRODUCTIVE ORGANS. 

THE UTERUS. 

Development and Anatomy. — The uterus is formed by the 
fusion of the middle portions of Midler's ducts, the fusion first oc- 
curring below where the cervix uteri is developed. The epithelial 
lining of the ducts gives rise to the mucosa of the uterus, and its 
outer layers to the muscularis. The utricular glands are devel- 
oped by ingrowths from the lining cells, and first appear and reach 
their most complex development in the cervical portion. The outer 
surface of the cervix (portio vaginalis) is lined with stratified squa- 
mous epithelium ; the cavity of the uterus and cervical canal with 
cylindrical ciliated cells. In the cervical portion are found nu- 
merous racemose glands and between them simple tubular glands ; 
in the corpus uteri the glands are simple tubules. 



DISEASES OF THE REPRODUCTIVE ORGANS. 



637 



CONGENITAL ABNORMALITIES. 

Absence of the uterus is very rare. The organ, however, may 
be represented only by a mass of rudimentary tissue. Hypoplasia 
of the uterus may be a congenital condition, or may be the result 
of arrested development and the consequent failure to increase in 
size at the age of functional activity. The term uterus foetalis seu 
infantilis is applied. Stenosis and atresia of the uterus and vagina 
may be the result of disease or maldevelopments, due to partial 
obliteration of Midler's ducts. 

Among the more striking malformations of the uterus are those 
which result from incomplete fusion of Midler's ducts. In nor- 




Fig. 303.— Uterus bicornis unicollis (Winckel). 



mal development these ducts unite and fuse in the lower portion 
to form the uterus and vagina, but remain separated above, where 
they form Fallopian tubes. Among the anomalous conditions of 
the uterus are uterus bicornis, in which the cervical portion of the 




Fig. 304.— Uterus septus (Cruveilhier). 



uterus is single, or two entirely distinct uterine cornua are present 
(Fig. 303) ; uterus septus, in which the external appearance may 
be that of a single uterus, but on section a septum is discovered, 
which divides the organ into lateral halves (Fig. 304). The term 



638 



TEXT-BOOK OF PATHOLOGY. 



uterus unicornis is used to designate cases in which but one of 
Mutter's ducts has developed, the other remaining rudimentary. 
Malformations of the vagina may be associated with those of the 
uterus already named, though this is rarely the case. A number 
of subdivisions have been distinguished for each of these malforma- 
tions, but they are unimportant. 

ALTERATIONS OF POSITION. 

The normal position of the uterus is one of slight anteversion 
with anteflexion ; that is, the fundus lies a little farther to the 
front than the cervix, and there is a slight band or flexure in the 
middle portion. 

Anteflexion is a condition in which there is marked angula- 
tion of the uterus, the fundus falling forward. Relaxation of the 
ligaments predisposes to this condition ; and it may be caused by 
the pressure of tumors situated posteriorly, by distention of the 
rectum with gas, by the traction of adhesions and by abnormal 
conditions of the uterus itself, causing a loss of tone in the walls. 
The grade of anteflexion varies greatly. Among the effects of 
this condition is interference with the discharge of menstrual 
blood, with consequent accumulation and intense dysmenorrhea. 

Anteversion, or the tilting forward of the uterus without 
abnormal angulation, occurs under similar conditions, but is less 
important. 

Retroflexion of the uterus occurs in cases in which the walls 
of the uterus are abnormally soft and have lost their tone. It 
may be caused by the pressure of tumors or the traction of adhe- 
sions. Sometimes it is due to habitual constipation, causing pressure 
of masses in the rectum upon the lower part of the uterus (cervix) ; 
retroversion and subsequently retroflexion are produced. Laxness 
of the vaginal walls and rupture of the perineum may cause this 
or other abnormal positions of the uterus by depriving the organ 
of its support from below and subjecting it to the unresisted press- 
ure of the abdominal viscera. The degree of retroflexion varies 
from slight angulation to a complete backward doubling of the 
organ. The fundus may undergo considerable congestion from 
the interference with circulation, and it is not rarely enlarged. 
Adhesions between the uterus and rectum are frequent. 

I/ateral displacements of the uterus are rare. 

Upward dislocation may be caused by pressure of tumors 
in the pelvis ; it may be due to the traction of adhesions between 
the uterus and large tumors of the ovary. In such cases the 
uterus may be greatly stretched and the vagina may be similarly 
affected. 

Prolapse of the uterus is a term applied to descent or 
downward displacement. It is possible to distinguish any num- 



DISEASES OF THE REPRODUCTIVE ORGANS. 



639 



ber of degrees of prolapse, but it is sufficient to speak of two only : 
incomplete prolapse, in which the os uteri is still within the vagina, 
and complete prolapse, in which it projects through the vulva. 
The causes of prolapse of the uterus are numerous. Injuries to 
the perineal floor and unusual laxity of the vaginal walls or the 
ligaments of the uterus are very important. Traumatism and ex- 
cessive pressure upon the uterus from the abdomen may cause de- 
scent of the organ, especially if laxity of the ligaments was present 
before. Enlargement of the uterus itself may be the cause of pro- 
lapse, and in any case the organ usually becomes enlarged after 
the prolapse, in consequence of passive congestion. The cervix is 
generally directed somewhat backward, and the mucous membrane 
frequently presents catarrhal inflammation and contains enlarged 
veins. The cavity may be filled with considerable mucous secretion. 

In some instances of apparent complete prolapse the fundus of 
the uterus may be but little displaced, the great descent of the os 
uteri in such instances being due to hypertrophic elongation of the 
vaginal portion o f the cervix. 

In all cases of prolapse the anterior and posterior walls of the 




Fig. 305.— Complete prolapse of the uterus (Penrose). 



vagina are displaced downward more or less, and sometimes may 
be completely everted. The anterior vaginal prolapse may draw 
Avith it the posterior wall of the bladder, and cystocele results. 
Similarly the posterior vaginal wall may drag down the anterior 
wall of the rectum, and rectocele is produced (Fig. 305). 



640 



TEXT-BOOK OF PATHOLOGY. 



Inversion of the Uterus is a condition in which the organ 
is turned inside out to a greater or less extent. This condition is 
caused by traction upon the placenta during labor, when it is 
acutely developed ; or by the similar traction of polypoid sub- 
mucous tumors, when it is more slowly formed (Fig. 306). There 




Fig. 806.— Fibroid polyp, producing partial inversion of the uterus (Penrose). 

may be only a slight inversion of the fundus, or the organ may be 
completely inverted and may present itself through the vagina and 
vulva. Secondary changes are apt to occur in such cases. The 
mucous membrane suffers catarrhal inflammation with ulceration ; 
and the entire uterus, though at first perhaps enlarged by conges- 
tion, subsequently atrophies. 

STENOSIS, DILATATION, AND RUPTURE. 

Stenosis of the uterine cavity may occur as a congenital con- 
dition, or may be acquired in cases in which inflammation has 
led to cicatricial stricture. There may be almost complete obliter- 
ation of the external or internal os uteri. 

Dilatation of the cavity of the uterus is a not infrequent 
result of stenosis. The dilated cavity may be filled with mucus 
or seromucous secretion from the mucous membrane (hydrometra), 
or with accumulations of menstrual blood (hematometra). 
Occasionally in cases of hydrometra secondary decomposition of 
the liquid causes gas-formation, and physometra results. In cases 
of hematometra the amount of blood in the uterine cavity may be 



DISEASES OF THE REPRODUCTIVE ORGANS. 



641 



very considerable, and in some instances rupture of the wall of the 
uterus is the result. This may be simply due to the increasing 
pressure, or it may result from inflammation or ulceration at the 
point of stenosis. 

Rupture of the uterus may occur during pregnancy or labor ; 
and occasionally at other times in consequence of inflammations, 
abscess, softened tumors, and the like. The most frequent and 
serious consequence of rupture is peritonitis. Occasionally, when 
rupture has occurred during pregnancy, the fetus may be enclosed 
in a sac formed by circumscribed peritonitis ; the rupture may at 
the same time heal. Subsequently the fetus may be disorganized 
and discharge through the abdominal wall. This is a very unusual 
termination. 

Laceration of the cervix uteri is a very common accident of labor. 

CIRCULATORY DISTURBANCES. 

Hyperemia of the uterus is a physiologic condition during 
menstruation, and occurs in all forms of acute inflammation of the 
organ. There is no essential difference between menstrual hyper- 
emia and that of pathologic conditions. 

Menstruation. — Examination of the mucous membrane during 
the period shows swelling of the membrane, with multiplication 
of the interglandular cells and dilatation of the lymphatic chan- 
nels. The uterine glands are elongated and the cells more or less 
swollen. Congestion is always conspicuous, and the superficial 
epithelial cells are desquamated more or less considerably. In 
the interval between the periods regeneration of the mucous 
membrane takes place. The term dys- 
menorrhea membranacea is applied to 
abnormal menstruation in which mem- 
branous formations are discharged from 
the uterus (Fig. 307) and in which there 
is severe pain. The membranes consist 
of intact portions of desquamated cells 
more or less degenerated. Cases of this 
character are particularly prone to occur 
when chronic inflammations of the mu- 
cosa have existed, and the affection is 
then termed endometritis exfoliativa. 

Passive hyperemia of the uterus 
occurs in conditions of general venous 
stasis, but especially when dislocations 
of the uterus cause pressure upon the 
venous plexuses. The organ is enlarged, 
the veins in the serous surface are 
prominent, the mucous membrane is dark red, and when the con- 
gestion is long continued chronic endometritis may result. 

41 




Fig. 307.— Membrane dis- 
charged in membranous dys- 
menorrhea (Penrose). 



642 



TEXT-BOOK OF PATHOLOGY. 



Hemorrhages may occur into the uterine cavity, into the Avail 
of the uterus, or into the peritoneum outside the uterus. Hemor- 
rhages during menstruation and in labor are physiologic forms. 
Pathologic increase of menstrual hemorrhage is spoken of as 
menorrhagia, which may occur in certain general diseases, such as 
anemia, or in consequence of local conditions, notably tumors. 
Intense congestion of the organ from cardiac disease or from mal- 
positions of the uterus may also lead to hemorrhages during the 
menstrual period. Hemorrhages between the menstrual periods 
are spoken of as metrorrhagia. This may be caused by general 
conditions, such as the hemorrhagic diseases, and infections (small- 
pox, etc.) ; but it is especially frequent as a result of local diseases, 
of which fibroid tumors are the most important. 

Hemorrhages into the substance of the uterus are rare, and are 
generally due to traumatism. 

Hemorrhages into the peritoneal cavities or into the cellular 
tissues in the vicinity of the uterus are more frequent. Of the 
intraperitoneal hemorrhages the most frequent is accumulation of 
blood in Douglas's pouch {retro-uterine hematocele). The blood in 
this case may come from various sources, such as ruptured ovarian 
follicles, ruptured tubes in tubal pregnancy, hematosalpinx, or 
rupture of varicose veins in the broad ligament. The blood may 
become absorbed without causing other pathologic results, or it 
may set up inflammation and result in adhesions between the 
uterus and rectum. Not rarely perforation with discharge of 
the blood through the rectum or vagina occurs. 

Hemorrhages into the vesico-uteriue pouch and hematoma 
between the layers of the broad ligament are rare. 

INFLAMMATIONS. 

Inflammation may affect the mucous membrane of the uterus, 
when the term endometritis is applied, or the wall of the uterus, 
when it is termed metritis. The names perimetritis, indicating 
inflammation of the peritoneal covering of the uterus, and para- 
metritis, inflammation of the cellular tissues in the vicinity of the 
uterus, are unnecessary, as these conditions are simply forms of 
local peritonitis. For purposes of convenience the inflammations 
of the uterus occurring during the puerperium will be separately 
considered. Some of the conditions here described as inflamma- 
tory are not positively of such nature, though no sharp line of 
division can be drawn between the inflammatory and the hyper- 
plastic forms. 

Acute catarrhal endometritis may result from trauma- 
tism, or from infection with pyogenic organisms or gonococci. 
Occasionally it occurs as a complication of general infectious 
diseases, such as typhoid fever and cholera. The mucous mem- 
brane is swollen and intensely hyperemic ; very often small hemor- 



DISEASES OF THE REPRODUCTIVE ORGANS. 643 



rhages are observed. Desquamation of the epithelial cells, with 
mucopurulent secretion, causes considerable discharge. In most 
cases the body of the uterus is affected, but in the gonorrheal form 
the cervical portion is the most frequent seat. Very intense forms 
may occasion necrosis of the epithelial cells and the formation of 
pseudomembranous deposits. This is particularly frequent in the 
infectious diseases. 

Chronic endometritis may be the continuation of acute 
endometritis, and is especially apt to occur in persons of reduced 
vitality, such as scrofulous or chlorotic women, or in those in 
whom the circulation is sluggish. The influence of passive con- 
gestion has already been referred to. Very often the etiology is 
entirely obscure. 

The mucous membrane in the earlier stages is simply swollen, 
and produces abundant mucopurulent secretion. Later, hyper- 
plastic changes occur, the hyperplasia affecting either the uterine 
glands or the interstitial tissue. The terms endometritis glandu- 
laris and endometritis inter stitialis have been applied to distinguish 
these varieties. In the former, microscopic examination shows an 
abundance of proliferated glandular acini extending through the 
depth of the mucous membrane (Fig. 308). In the latter the 




Fig. 308.— Glandular endometritis 



glands are less conspicuous, but round-cell infiltration and abun- 
dant connective-tissue hyperplasia between the glands are con- 
spicuous features (Fig. 309). In some of the cases, particularly 
in those of the glandular form, the process seems more closely 
allied to tumor-formation than to inflammation ; and it is very 
difficult to draw a sharp line between some forms of adenoma 
and sarcoma of the mucous membrane on the one hand, or chronic 



644 TEXT-BOOK OF PATHOLOGY. 

inflammations on the other hand. The mucous membrane mav in 




Fig. 309.— Interstitial endometritis. 



the advanced stages be considerably swollen and project in a poly- 
poid form (Fig. 310). Later, atrophy may take the place of hyper- 
trophy, and in some instances the lining epithelial cells change 



if _ 



j mm? < 

Fig. 310.— Polypoid endometritis (Penrose). 



their character from the typical columnar cells to a distinct 
squamous type. The small glands of the membrane may be 
obstructed at their mouths and cystic distention may result. This 
is particularly conspicuous in the case of the Nabothian glands of 
the cervix, and retention-cysts of these glands may reach the size 
of a pea or a small cherry. Occasionally erosions or slight ulcer- 
ations are met with in cases of chronic endometritis. 



DISEASES OF THE REPRODUCTIVE ORGANS. 645 



Chronic endometritis of the cervix is frequently secondary to 
inflammations of the vagina, and may be due to gonorrheal infec- 
tion or other causes. The mucous membrane of the cervical canal 
is greatly thickened, and may project from the os uteri (ectro- 
pium). Retention-cysts of the Nabothian glands are sometimes a 
conspicuous feature ; and cystic mucous polyps are not unusual. 

Chronic endometritis may lead to chronic metritis, or by exten- 
sion may occasion tubal disease. Clinically it is characterized by 
more or less constant mucopurulent discharge. 

Erosions of the uterus are especially frequent in the cervix ; 
they result from endometritis. The mucosa within the cervical 
canal undergoes hyperplastic changes and projects from the os 
uteri in a polypoid form. Between the papillomatous projections 
cystic formations may develop, and these may rupture, leaving 
exposed ulcerations. Granulation-tissue is developed from the 
submucosa, and sometimes this becomes exuberant in character. 




Fig. 311. — Left lateral laceration of the cervix, with erosion (Penrose). 

The term " erosion " is also applied to areas in which the normal 
squamous epithelium of the cervix has become converted into 
cylindrical, or in which the cylindrical epithelium of the body of 
the uterus has extended downward to the cervix. Other erosions 
are due to laceration of the cervix (Fig. 311); and occasionally 
congenital erosion has been observed. 

Phagedenic ulceration of the cervix has been described as an 
independent disease. Some of the cases are undoubtedly instances 
of ulcerating carcinoma ; in other cases ulcerations in this situa- 
tion have been met with in which microscopic examination showed 
no evidence of carcinomatous tissue. 

Acute metritis is rarely met with, except during the puer- 
perium, but may be the result of acute endometritis. The wall 



646 



TEXT-BOOK OF PATHOLOGY. 



of the uterus becomes thickened, soft, and edematous. Occasionally 
purulent infiltration is observed. 

Chronic metritis frequently occurs in the puerperium as a 
result of retarded involution of the uterus. It may be occasioned 
by chronic congestion of the uterus, or may be secondary to chronic 
endometritis. The uterine wall is infiltrated with round cells, 
and the connective tissues undergo active hyperplasia, which in 
the later stages leads to great thickening and induration. Coinci- 
dently there is usually some hypertrophy of the muscular elements 
themselves. It is by no means certain that all of the cases 
grouped under this term are inflammatory in nature. Some are 
certainly more closely allied with diffuse tumor-formation. The 
mucous membrane is usually thickened, and becomes secondarily 
involved if it was not primarily diseased. The peritoneal cover- 
ing may be similarly affected, and chronic perimetritis with adhe- 
sions of the uterus results. 

INFECTIOUS DISEASES. 

Puerperal Infections. — This term may be applied to vari- 
ous forms of infection occurring during the puerperium, but in 
the majority of instances the streptococcus is the specific organ- 
ism. 

Etiology. — Two important factors are concerned : (a) injuries 
to the surface of the uterus, vagina, or vulva ; and (b) some form 
of infection. The more or less denuded surface of the uterus of- 
fers a ready entrance to micro-organisms, as well as an absorptive 
surface for soluble poisons produced by micro-organismal decom- 
position within the uterus ; and infection may take place without 
any further injury than that occasioned by the normal processes 
of labor. In most instances, however, there is actual injury either 
of the surface of the uterus, cervix, vagina, or vulva, and the 
micro-organisms or poisons are admitted through these wounds. 
There may be primarily, however, more than a simple injury of 
the mucous surface. In consequence of prolonged pressure ne- 
crotic lesions terminating in gangrene may first be established, 
and from this secondary infections may take place. In cases in 
which infection occurs without injury to the walls, as well as in 
cases in which injury has been sustained, the pathogenic organisms 
may first find a lodgement and multiply within the blood-clots or 
retained secundines within the uterus ; and the organisms or their 
toxic products are secondarily admitted to the uterine tissues. 

Puerperal infection is probably in most cases the result of the 
entrance of micro-organisms from without, and may be traced to 
want of cleanliness on the part of the accoucheur or the surround- 
ings. Sometimes widespread epidemics have been caused by the 
carelessness of a single obstetrician, whose hands perhaps had be- 



DISEASES OF THE REPRODUCTIVE ORGANS, 647 



come infected from operating upon or examining cases of erysipelas, 
general pyemia, or the like. 

Among the micro-organisms, as has already been stated, the 
Streptococcus pyogenes is most important. Staphylococci of vari- 
ous sorts, bacilli resembling the Bacillus coli communis, the bacil- 
lus of tetanus, gonococci, and other organisms occasionally infect 
the puerperal uterus, but in these instances the pathologic condi- 
tions are different from those met with in ordinary puerperal infec- 
tion, which may be considered as practically always a streptococcic 
infection. 

Pathologic Anatomy. — rn most instances there is primarily a 
lesion upon the mucous surface of either the uterus, the vagina, or 
the vulva. The nature and extent of this depend upon the amount 
of injury occasioned during labor. In some instances the lesion is 
trivial in extent, and remains so, though widespread infection re- 
sults from it. In most cases, however, there is a rapidly spread- 
ing inflammation of the endometrium or mucosa of the vagina, and 
pseudomembranous deposits are very frequently met with upon 
the surface. Necrotic and gangrenous changes in the mucous 
membrane are most pronounced in cases in which prolonged press- 
ure has been exerted by the head in its descent or by instruments. 

The extension of the infection may occur in two ways, either 
through the blood-vessels or through the lymphatic channels ; and 
the local and general lesions vary correspondingly. 

In cases in which the infection spreads along the blood-vessels 
there may be primarily septic softening of the thrombi within the 
uterus and purulent phlebitis of the venous channels at the pla- 
cental site. Thrombosis extends from this situation through the 
veins to the various plexuses in the vicinity, and infected emboli 
are carried through the circulation to distant organs, such as the 
lungs, the kidneys, and the spleen. Metastatic abscesses and in- 
flammatory swelling of the affected organs result. The kidneys 
in particular are often the seat of numerous punctate or miliary 
abscesses. 

In the cases in which extension occurs along the lymphatic 
channels the uterus is enlarged, soft, and often pultaceous. Streaks 
or lines of light color may be observed running from the mucous 
surface toward the periphery. These represent the lymphatic 
vessels filled with purulent exudate. The walls of the lymphatics 
may be penetrated, and perilymphangitic abscesses are thus occa- 
sioned. When the process has extended to the lymphatics in the 
outer layers of the uterus phlegmonous inflammation of the sub- 
peritoneal tissues (parametritis) results, and finally the peritoneum 
itself may be involved. 

The spleen is enlarged, though less decidedly than in the form 
in which infection occurs through the blood-vessels. 

Extension along the mucous membrane itself may lead to asso- 



648 



TEXT-BOOK OF PATHOLOGY. 



LT 



ciated disease of the tubes ; more frequently the tubes are invaded 

at their abdominal end after 



peritonitis has developed. 

Puerperal sepsis is pecu- 
liarly virulent and rapid in 
its course, and may occasion 
widespread changes in all of 
the tissues of the body. 

Tuberculosis. — Tuber- 
culosis of the uterus is most 
frequently met with in the 
mucous membrane, and is 
usually secondary to disease 
of the tubes. Direct infec- 
tion may possibly occur 
through coitus ; but is cer- 
tainly rare. The disease 
occurs in the form of a 
nodular or diffuse infiltra- 
tion with a tendency to rapid 
ulceration or caseous necrosis 
involving the mucous mem- 




Fig. 312.— Diffuse tuberculosis (ulcerative and 
caseous) of the endometrium (Kaufmann). 



brane and to some extent the submucosa. The entire cavity of 
the uterus may be covered with caseous and necrotic deposits 




is 



Fig. 313.— Miliary tuberculosis of the endometrium and glandular endometritis (Beyea). 

(Fig. 312). In the later stages the process may extend deeply, 
even involving the muscular layer of the organ. The cervix 



DISEASES OF THE REPRODUCTIVE ORGANS. 



649 



is rarely attacked. Sometimes miliary tubercles are found in the 
uterine mucosa without marked degeneration (Fig. 313). 

Syphilis of the cervix uteri may occur in the form of a chan- 
cre, or as tertiary infiltration. 

ATROPHY AND DEGENERATIONS. 

Puerperal Atrophy. — The uterus suffers a most remarkable 
atrophy following labor. This proceeds very rapidly at first, and 
then more slowly ; and under favorable conditions the organ re- 
sumes its previous condition in the course of a few months. The 
muscular fibers decrease progressively, from their previous hyper- 
trophied condition, in which they frequently attain a length and 
diameter three times the normal, until, at the end of involution, 
the usual size and appearances are attained. Many muscle-fibers 
undoubtedly are destroyed. The process of involution is really 
one of fatty degeneration. 

Senile Atrophy. — The uterus undergoes progressive atrophy 
at and after the period of the menopause, and finally becomes 
greatly reduced in size. The substance of the organ may undergo 
a progressive sclerosis, or in other instances becomes softer than 
normal. Catarrhal endometritis is often associated, and the co- 
lumnar cells are sometimes converted into squamous epithelium. 

Fatty degeneration, independent of that which occurs dur- 
ing puerperal involution, is a rare condition, but may occur in the 
course of certain infectious diseases, such as typhoid fever, or may 
result from the action of the parenchyma-poisons. 

Amyloid degeneration is rare and unimportant. 

HYPERTROPHY AND HYPERPLASIA. 

Hypertrophy of the entire uterus may occur in association 
with inflammation or metritis, or may result from chronic conges- 
tion of the organ. The enlargement in cases usually designated as 
hypertrophied is, for the most part, due to new-formed connective 
tissue. True hypertrophy occurs as a physiologic process during 
pregnancy. In this variety the muscle-fibers increase enormously 
in size, and doubtless also multiply their number. The blood-ves- 
sels and connective tissues undergo corresponding hypertrophy. 

Hypertrophy of the cervix uteri is occasionally met with 
independent of hypertrophy of the uterus as a whole. It may be 
caused by chronic irritations of the cervix, as in cervical endome- 
tritis, or may result from obscure causes. Frequently it is met 
with in prolapse of the uterus, and sometimes it may cause a 
simulation of prolapse. 

Hyperplasia of the mucous membrane of the uterus has 
been referred to in the discussion of chronic endometritis. In 



650 



TEXT-BOOK OF PATHOLOGY. 



some instances that are designated as endometritis the pathologic 
process seems to be rather of a purely hyperplastic character, and 
more closely allied to tumor-formation than to ordinary inflam- 
mation. In these cases the mucous membrane in all parts of the 
uterus may be greatly thickened, and may suffer more or less 
papillomatous transformation. Sometimes limited portions are 
affected, and polypoid formations result. 

Polyps of the uterus may be of various sorts. Very com- 
monly they present themselves as simple mucous polyps, due to 
projection of parts of the mucous membrane ; in other cases sec- 
ondary changes, such as cavernous dilatation of the blood-vessels 
or cystic transformation of the small glands contained in the polyp, 
occasion marked variations from the original appearances. Myo- 
fibromata, sarcomata, and other forms of tumors originating in the 
mucous membrane or just beneath it may assume a polypoid 
appearance. 

TUMORS. 

leiomyoma ; Myofibroma ; Fibroid. — The tumors of the 
uterus designated by these terms are in nearly all cases composed 
of smooth muscle-fibers and fibrous tissue ; and from the patho- 
logic standpoint the term myofibroma is therefore most applicable. 
They present themselves in the form of rounded and usually well- 
circumscribed masses, from the size of a grape-seed to that of 
tumors weighing forty or fifty pounds. They are generally mul- 
tiple ; are very hard ; and on section have the appearance of con- 
centric or irregular lamella?. Microscopically the tumor is com- 
posed of smooth muscle-fibers and of fibrous tissue arranged in 
bundles or layers running in various directions. The muscle- 
fibers are frequently found arranged concentrically about small 
blood-vessels, and in some instances the vessels are telangiectatic. 

Secondary changes are very common, the most frequent being 
calcification. This may begin either in the center or at the 
periphery, but more commonly it is diffuse. Edema of the tumor 
may cause it to become quite soft, and cystic transformations due 
to softening or to distention of the lymphatic spaces are sometimes 
observed. 

Several varieties have been distinguished, according to the seat 
of the tumors. In some instances they are embedded in the wall 
of the uterus, when the term interstitial or mural fibroids is applied 
(Fig. 314). In other cases they arise in the uterine walls just beneath 
the mucous membrane, when they are called submucous fibroids. 
These may gradually project into the cavity of the uterus as fibroid 
polyps. In the third group of cases the tumors have a subperito- 
neal location, and may project from the outer surface of the uterus 
as knobbed masses (Fig. 315), which may become pedunculated. 
In rare instances they extend between the layers of the broad liga- 



DISEASES OF THE REPRODUCTIVE ORGANS. 651 

ment. Fibroid tumors are benign in a pathologic sense, but occa- 
sion serious disturbances either by pressure or by the metrorrhagia 




Fig. 314.— Interstitial fibroid tumor of the uterus : a small submucous fibroid appears in 
the uterine cavity (Penrose). 



and endometritis to which they frequently give rise. Subperitoneal 
fibroids may become free bodies in the peritoneal cavity, and the 




Fig. 315— Subperitoneal fibroids and an intraligamentous fibroid of the uterus (Penrose). 



submucous form is sometimes discharged from the uterus after a 
spurious labor. 



052 



TEXT-BOOK OF PATHOLOGY. 



Sarcoma of the uterus may arise from the muscular layer or 
from the endometrium. That arising from the myometrium is 
usually associated with myoma and fibroma. In some cases the 
sarcomatous elements of the tumor are developed in a pre-existing 
myofibroma. In other cases the sarcoma and fibroma are coinci- 
dentally formed. These tumors differ from typical fibroids in 
being more rapid in growth, less well circumscribed, softer, and 
more homogeneous in appearance. Sometimes they are situated 
just beneath the endometrium, and become converted into sarcom- 
atous polyps. 

Sarcoma of the endometrium may occur in a circumscribed or 
papillomatous and in a diffuse form, the latter involving the entire 
mucous membrane of the organ. The papillomatous variety is 
soft and villous and highly vascular. In some cases the structure 
is that of angiosarcoma. In the diffuse form the entire cavity of 
the uterus may be filled with soft villous projections from the 
mucous membrane. 

A special form of sarcoma has been described as occurring in 
the vaginal portion and cervix. In this the tumor has a grape- 
like structure, and microscopically consists of myxomatous tissue 
with areas of sarcomatous character. It occurs in young persons, 
even in childhood. 

Adenoma. — Adenoma may occur in the form of polypoid out- 
growths from the mucous membrane, or as a diffuse process not 
readily distinguishable from that commonly designated as endo- 
metritis glandularis. Both of these forms are benign. 

Malignant adenoma usually arises from the corpus uteri, 
and presents itself as a soft, irregular elevation of the mucous 
membrane in a localized area, or diffusely involving a large part 
of the endometrium. It tends to spread through the walls of the 
uterus, invading the myometrium (Fig. 316) and finally penetrating 
to the peritoneal covering, where secondary nodules may develop. 
Histologically it is characterized by the production of atypical 
branched gland-acini with comparatively little stroma, the latter 
being of soft fibrous character. The tumor is malignant in its 
tendency to invade the wall of the uterus and neighboring struct- 
ures, and it may become converted into actual carcinoma in the 
later stages. In such instances the acini in places show a heaping 
of epithelial cells and a tendency to destruction of the basement- 
membrane, with proliferation of the cells in the stroma. 

Carcinoma. — Carcinoma is the most frequent of the malig- 
nant diseases of the uterus, and usually invades the cervical 
portion ; more rarely it arises from the corpus uteri. Carcino- 
mata starting on the vaginal surface of the cervix are squa- 
mous-celled epitheliomata ; those originating in the cervical canal 
and in the corpus uteri are tubular or glandular carcinomata. 

Carcinoma of the portio vaginalis usually begins from the 



DISEASES OF THE REPRODUCTIVE ORGANS. 653 

inner surface of one of the lips of the os uteri, and causes a firm 
infiltration of the affected portion, the disease penetrating into the 




Fig. 316. — Malignant adenoma : the section is taken from the deeper parts of the tumor, 
and shows the invasion of the myometrium. 

submucosa and muscularis. Subsequently ulceration takes place, 
and the diseased area becomes converted into an elevated and 




Fig. 317.— Diffuse cancer of the endometrium (Penrose). 



irregularly ulcerated surface. Extension may take place to the 
vaginal walls and to the tissues surrounding the cervix uteri. 



654 



TEXT-BOOK OF PATHOLOGY. 



Ulceration may establish communications between the vagina and 
bladder or rectum. Extension upward into the supravaginal 
portions of the cervix and to the corpus uteri may occur through 
the lymphatic channels, or by direct invasion. Secondary involve- 
ment of the lymphatic glands of the iliac, lumbar, and inguinal 
groups is frequent. 

Instead of the usual indurated and ulcerating form, cervical 
epithelioma may present itself as a cauliflower-growth — that is, as 
a destructive or malignant papilloma. In such cases it is likely 
that the growth often begins as a papilloma, causing irregular 
elevations, and that the penetration into the tissue at the base of 
the growth is a secondary development. In the later stages this 
form, like the preceding, undergoes ulceration. Both varieties, 
but particularly the latter, frequently cause uterine hemorrhages. 

Carcinoma of the corpus uteri and of the cervical canal 
develops from the tubular and acinous glands of the mucous 
membrane. It may begin as an adenomatous growth, subse- 
quently becoming transformed into carcinoma. Macroscopically 
the growth presents itself as a villous or papillomatous thickening 
of the mucosa, either localized or diffuse (Figs. 317 and 318). In 




Fig. 318.— Cancer of the body of the uterus : a large, single cancerous nodule in the 
anterior wall has been divided (Penrose). 



the later stages considerable involvement of the wall of the uterus 
occurs, and even perforation may take place. Microscopically the 
usual appearances of glandular cancer or adenocarcinoma are 
discovered (Fig. 319). 

Squamous epithelioma is met with in rare instances in the 
corpus uteri, especially in women of advanced years. The ex- 



DISEASES OF THE REPRODUCTIVE ORGANS. 655 



planation of this growth is that it arises from epithelium that has 
undergone a change from the customary columnar to the squamous 
form, in consequence of chronic endometritis. 




Fig. 319.— Glandular cancer of the cervix uteri. 



Cysts. — Small cysts of the wall of the uterus may be asso- 
ciated with various forms of tumors, such as myofibromata ; and 
a form of adenocystoma, probably originating from remnants of 
the Wolffian duct, has been described. Dermoid cysts have been 
occasionally observed. 

PARASITES. 

Echinococcus-cysts are sometimes met with, and a few cases of 
supposed Cysticercus cellulose have been described, though the 
nature of the formations was uncertain. 



THE OVARIES. 

Development and Anatomic Considerations. — The 

ovary and testis are developed from a primary indifferent sexual 
gland, which is indistinguishable in the two sexes. This indiffer- 
ent gland is formed on the ventro-mesial surface of the Wolffian 
body by a localized thickening of the mesothelial elements. The 
ovarian stroma is subsequently formed by ingrowths of the sur- 
rounding mesoderm. The ovary consists of a stroma of peculiar 
spindle-shaped connective-tissue cells. In the central or medullary 
portion the tissue is highly vascular ; the peripheral or cortical 
part contains abundant Graafian follicles in which the ova are de- 



656 



TEXT-BOOK OF PATHOLOGY. 



v eloped. These follicles are formed from primary tubular inden- 
tations of the cuboidal or columnar epithelium that covers the 
organ. These indentations are the tubes of Pfliiger. After full 
development of the ovary they are wanting, the greater part by 
constriction of the deeper portions having formed primordial 
follicles. The paroophoron, a vestigial structure, is the part of the 
ovary at the hilum. It consists of connective tissue and blood- 
vessels with a number of parallel tubes which are remnants of 
the Wolffian body. The same tubules surrounded by connective 
tissue extend outward between the layers of the broad ligament, 
constituting the parovarium. Sometimes part of the Wolffian 
duct remains patulous and constitutes the duct of Gartner. This 
is the homologue of the vas deferens. 

CONGENITAL ABNORMALITIES. 

Occasional absence of one or both ovaries has been discovered 
with other developmental defects, or independently. Hypoplasia 
occurs in chlorosis, and occasionally in association with other con- 
ditions. Sometimes supernumerary ovaries have been found. 
The additional ovaries may be formed by division or by separa- 
tion from one of the normal glands. 

CHANGES IN POSITION. 

More or less extensive dislocations of the ovaries may occur, 
the most notable being that in which one of these organs descends 
into a hernial sac, occupying either the inguinal or crural canal. 
Dislocations resulting from pressure, adhesions, and the like are 
frequent. 

CIRCULATORY DISTURBANCES. 

Active hyperemia, or congestion, may be either a physi- 
ologic or pathologic condition. The former occurs during the 
menstrual period, the latter in association with inflammation of 
the neighboring structures or in the earlier periods of inflamma- 
tion of the ovaries themselves. 

Passive congestion is met with in chronic cardiac diseases, 
and as a result of local obstructions to the circulation by tumors, 
inflammatory adhesions, and the like. 

Hemorrhage. — Small hemorrhages into the ovarian tissue are 
very frequent. Their occurrence is usually sufficiently accounted 
for when the functional activity of the organ is considered. At 
each periodical ovulation a small follicle ruptures, to discharge the 
contents containing the ovum. Generally there is a slight extrav- 
asation of blood at such times, which is subsequently absorbed. 
At the same time that the extravasation and absorption are taking 
place the inner lining of the follicle proliferates somewhat, and 



DISEASES OF THE REPRODUCTIVE ORGANS. 



657 



the cells then undergo fatty degeneration. The whole process 
gives rise to a yellowish nodular formation, termed the corpus 
luteum. Subsequently this is removed by absorption of the blood 
and by degeneration and absorption of the proliferated cells 
of the lining membrane, and a small scar alone remains. The 
latter, especially when more than usually fibrous, is known as the 
corpus fibrosum. This is commonly a little pigmented, in conse- 
quence of the pre-existing extravasation of blood. The corpus 
luteum, which is developed from a follicle formed at the time of 
impregnation (corpus luteum of pregnancy), differs somewhat in 
character. The epithelial proliferation is much more active, and 
the wall of the follicle is intensely congested. Rapid involution 
does not take place, the follicle often persisting for considerable 
periods after the termination of pregnancy. 

Exceptionally, considerable hemorrhages may take place into 
the follicles, and small hemorrhagic cysts or cysts containing 
blood-stained liquid may be formed. 

INFLAMMATION. 

Inflammation of the ovaries, or oophoritis, is generally 
a secondary condition resulting from an extension of inflammation 
from the neighboring reflections of the peritoneum, or from exten- 
sion of infective processes along the Fallopian tube. The exten- 
sion from the neighboring peritoneum, as well as from the uterus, 
may be direct — that is, along the planes of tissue or through the 
lymphatic or vascular channels. Acute oophoritis is not infre- 
quent in various forms of general infection, such as typhoid fever, 
pneumonia, influenza, etc. Primary oophoritis is probably very rare. 

The ovary becomes enlarged, and in the earlier stages is more 
or less congested. Later the tissues become yellowish, either 
uniformly or in scattered areas. Finally the process may termi- 
nate in necrosis or abscess-formation. Such ovarian abscesses 
may reach a considerable size, and break into any of the hollow 
viscera near by or into the peritoneal cavity. In more favorable 
cases there are only small collections of pus, and these may subse- 
quently become inspissated. The most satisfactory of all termi- 
nations is in complete resolution, or in induration (chronic 
oophoritis). 

Localized inflammations may sometimes occur about the folli- 
cles. These may terminate in follicular abscesses, which either 
discharge and lead to scar-formation, or become inspissated. 

INFECTIOUS DISEASES. 

Tuberculosis. — Among the infectious diseases tuberculosis 
alone is of importance. It may arise as a primary disease of the 
ovaries, but much more frequently is secondary to inflammation 

42 



658 



TEXT-BOOK OF PATHOLOGY. 



of the tubes or other parts of the genital tract. It may give rise 
to the formation of small or large cheesy masses, showing a ten- 
dency to softening with formation of tuberculous abscesses. The 
ovaries may occasionally be the seat of miliary tuberculosis. 

TUMORS. 

The ovaries are frequent seats of tumors, both benign and 
malignant. By far the largest proportion are cystic. 

Connective-tissue Tumors. — Fibromata may occur as small 
nodular growths, either single or multiple. In some cases the 
tumors are of considerable size. Combinations of fibroma with 
leiomyoma may also be met with ; these myofibromata resemble 
those of the uterus. Occasionally fibrosarcom a is encountered. 

Chondroma is a rare form of benign tumor. 

Sarcoma may occur in the form of spindle-celled sarcoma, 
fibrosarcoma, or more rarely as round-cell sarcoma. It appears 
as rounded tumors with more or less pronounced encapsulation. 
Degenerations, such as myxomatous, are not infrequent, and cystic 
change may be occasioned by dilatation of the follicles. In some 
cases proliferations of the walls of the follicles constitute an im- 
portant part of the growth. To such cases the name adenosarcoma 
may be applied. Angiosarcomata and endotheliomata have 
occasionally been described. 

Cystic Tumors. — Of the cystic conditions of the ovary we 
must distinguish the simple follicular cysts and the more important 
myxoid or colloid cystomata and dermoid cysts. Of the cystomata 
there are two varieties — the papillary and the glandular. 

Follicular cysts are developed by distention of the Graafian 
follicles with dropsical liquid. The ovary may be considerably 
enlarged by cystic cavities, lined with epithelium and containing 
clear watery liquid, or occasionally blood-tinged contents. Cysts 
of this character are very common in cases of induration of the 
ovary following oophoritis. 

Colloid or Myxoid Cystomata. — Colloid or myxoid cystomata 
present themselves as tumors of small or large size, having a 
tendency to a multilocular cystic character. The cavities are filled 
with a more or less gelatinous or mucoid liquid. Sometimes 
hemorrhage takes place, and the contents are correspondingly 
altered. Two subvarieties may be distinguished : the glandular 
and the papillary. 

Glandular cystomata are distinguished by the constant prolif- 
eration of the epithelial elements in the form of acini. This occa- 
sions a multilocular character, new cysts springing from the walls 
of the original cavity or appearing within the substance of the pri- 
mary tumor. The terms adenocystoma and cysto-adenoma are 
appropriate. The tumor may present itself as a large, single, 



DISEASES OF THE REPRODUCTIVE ORGANS. 659 



rounded, cyst with insignificant projections of small cysts upon the 
inner lining ; while in other cases there is found on section a uni- 
form multilocular character. Microscopically the characteristic 
feature of these tumors is the formation of regular, gland-acini, 
showing a single layer of epithelial cells, or at most a few layers 
resting upon a basement-membrane. The stroma of the tumor is 
composed of fibrous connective tissue, with some unstriped muscle- 
fibers. The contents of the cysts have the mucoid or colloid char- 
acter referred to, and chemically a substance is discovered that is 
absent from simple follicular cysts of the ovary and is less abun- 
dant in papillary cystomata. This substance is termed pseudo- 
mucin or paralbumin, and is somewhat related to mucin. 
Occasionally, when the cysts are old the contents may be quite 
watery. 

Cystomata soon destroy the ovary, the unaffected ovarian tissue 
being spread out within the wall of the cyst. The tumor is 
attached in the pelvis by a pedicle consisting of the broad liga- 
ment and Fallopian tube, and often forms secondary inflammatory 
adhesions to adjacent parts. 

Glandular cystomata arise either from embryonal rests (Pfluger's 
tubes), or from ingrowths of the surface-epithelium of the organ. 
It is generally considered unlikely that they arise from Graafian 
follicles. 

Papillary Cystomata. — Papillary cysts occur in two forms, 
the one closely resembling glandular cystoma in its general appear- 
ance, the other presenting itself as a papillomatous condition of the 
surface of the ovary. In the former, or papillary myxoid cysto- 
mata, large cystic tumors are developed. On section through these 
there is found a papillomatous or cystic proliferation of the lining 
membrane, but the tendency to the formation of secondary cysts 
is much less pronounced than in the glandular varieties, and the 
fibrous stroma is less abundant. The secondary cysts in this 
variety may be formed by fusion of the free ends of proliferat- 
ing papillae, or by myxomatous degenerations within the stroma 
of the papillae. The liquid of the cysts resembles that of the 
glandular form, but contains less pseudomucin, and is more fre- 
quently hemorrhagic. On microscopic examination it is found 
that the inner lining of the cyst and the papillary projections con- 
sist of stratified ciliated epithelium. Calcareous bodies arranged 
in a concentric fashion (psammoma-bodies) are frequently met 
with in the stroma, as well as in the epithelium. The same 
calcareous bodies are occasionally found in glandular cystomata. 

The papillomatous ovarian tumors differ from the glandular in 
being almost invariably bilateral (Fig. 320). Their origin has not 
as yet been certainly determined, but it is probable that they origi- 
nate from the paroophoron, a vestigial remnant of the parovarium. 
Some have held that they may originate from the Graafian follicles, 



660 



TEXT-BOOK OF PATHOLOGY. 



or from ingrowths of the surface-epithelium. This is assuredly 
not a frequent origin. 

The surface-papillomata of the ovary present themselves as ir- 
regular masses of a cauliflower appearance. The papillae of pro- 
jections are covered with ciliated epithelium, as in the cystic form. 
There is no essential difference in structure, and it is probable 




Fig. 320.— Double papillomatous cyst of the ovary : the right cyst has ruptured and is 
turned inside out, showing a mass of papillomata ; papillomata have penetrated the wall 
of the-cyst; the peritoneum has been infected, and a papillomatous growth appears on 
the fundus uteri (Penrose). 

that in most instances the superficial forms result from a rupture 
of the cystic variety and the subsequent external proliferation. 

The papillomatous cystomata and the surface-papillomata have 
a marked tendency to carcinomatous transformation, and tend to 
spread to the peritoneum, causing metastatic nodules in the 
vicinity or throughout the entire abdomen. 

Dermoid Cysts. — Dermoid cysts are frequently met with in the 
ovary. They may occur as small nodules or as very large tumors, 
and are usually unilateral. The larger ones substitute the ovarian 
tissue completely ; less commonly they may be pedunculated, the 
ovary in part remaining intact. Combinations with glandular 
cystomata are not infrequent. 

The dermoid cyst is a smooth-walled sac, the inner surface pre- 
senting somewhat irregular projections and having more or less 
pronounced characteristics of epidermal tissue. The cystic con- 
tents are a putty-like material of grayish color, containing long, 
blonde hairs and teeth, and sometimes ill-developed bone. The 
grayish material consists of fatty detritus containing degenerated 
epithelial cells, and usually abundant cholesterin-crystals. The 
wall of the dermoid cyst, though usually in the main composed 
of epidermal structure, may contain elements of the three blasto- 
dermic layers. The dermoid cyst may occur in childhood, or even 
in fetal life, but usually does not present itself till adult years. 

The nature of the tumor has not been certainly determined, 



DISEASES OF THE REPRODUCTIVE ORGANS. 



661 



but it is quite evident that it represents an attempt at the for- 
mation of an organism. It has, therefore, been designated by 
some as a foetus in foetu. Others have looked upon it as the result 
of a form of pathogenesis. 

Secondary changes not infrequently occur. Inflammatory con- 
ditions of the walls may occasion abscess. Sometimes the epithe- 
lium proliferates actively, and the dermoid, in part or as a whole, 
is converted into a carcinoma. 

Carcinoma. — Carcinoma of the ovary may be a primary 
growth of glandular character developing from the follicles, or it 
may be of a mucous or colloid variety, when the ovarian tissue 
becomes converted into a gelatinous mass. In the latter case the 
tumor tends to spread to the adjacent peritoneum, and widespread 
metastasis along this membrane may occur. 

CYSTS OF THE PAROVARIUM. 

Cysts of the parovarium may be considered in this place on 
account of their clinical resemblance to ovarian cystomata (Fig. 
321). They are distinguished, however, by their intraligamentous 




Fig. 321— Cyst of the parovarium : there is no distortion of the ovary ; the Fallopian tube 
has been much elongated. 

situation, by their almost invariably unilocular character, and 
usually by their clearer and more serous liquid contents. The 



662 TEXT-BOOK OF PATHOLOGY. 

ovary is usually uninjured. The inner lining consists of ciliated 
epithelium. 

CYSTS OF KOBELT. 

These are thin-walled, pedunculated cysts about the size of a 
pea (Fig. 322). They are frequently met with, and are seated at 




Fig. 322.— Fallopian tube, ovary, and parovarium : a, hydatid of Morgagni ; b, cyst of 
Kobelt's tube ; c, Gartner's duct (Penrose). 

the side of the ovary. The wall is fibrous, the lining membrane 
composed of cubical epithelium, and the contents a clear serous 
liquid. The cyst results from distention of one of Kobelt's tubes 
in the parovarium. 

THE FALLOPIAN TUBES. 

Development and Anatomy. — The tubes are formed from 
the upper ends of Miiller's ducts. The lower ends of the ducts 
fuse to form the uterus and vagina. Each tube is covered by a 
peritoneal coat, and its walls consist mainly of longitudinal and 
circular muscle-fibers. The mucosa is thrown into well-marked 
longitudinal plications, which at the uterine end are further com- 
plicated by secondary elevations. The epithelial lining consists 
of columnar ciliated cells. 

CONGENITAL ABNORMALITIES. 

The tubes may be absent or may be defective. Congenital 
atresia is occasionally observed. The tubes may be unusual in 
length and may communicate with the uterus in abnormal situ- 
ations. 

CHANGES OF POSITION. 

In dislocations of the ovaries the tubes are correspondingly dis- 
located. Independent of displacements of the ovary, the tubes 



DISEASES OF THE REPRODUCTIVE ORGANS. 



663 



may be distorted or pulled out of their usual position by inflam- 
matory adhesions, and may thus be bent at sharp angles or bound 
down in various malpositions. 

STENOSIS. 

Congenital stenosis of the tubes, or complete closure of the la- 
men, may affect the entire length of the tube or a limited portion, 
principally near the middle. Acquired stenosis may result from 
pre-existing disease of the tube itself, or from adhesions secondary 
to localized peritonitis. The most frequent situation in these in- 
stances is the abdominal or fimbriated end. A narrowing of the 
lumen of the tube may be occasioned by angulation or by disloca- 
tions. 

DILATATION. 

Dilatation on the proximal side of obstructions or stenosis is 
frequent. The dilatation is more marked when inflammatory con- 
ditions of the mucous membrane are present. The abdominal end 
of the tube may enlarge so as to form a cyst of considerable size, 
filled with serous or seromucous liquid, when the middle portion is 
stenotic. When the lower end is obstructed the entire tube be- 
comes dilated, and it frequently shows a tortuous and irregularly 
pouched condition, due to its attachments to the broad ligament. 
In such instances the mucous membrane is pushed inward at the 
bends, and projects prominently into the lumen of the tube. 
Secondary changes of the epithelial lining are not unusual in con- 
sequence of the irritation of the retained secretions. The normal 
epithelium may be wholly lost, and the lining may consist of squa- 
mous epithelial cells. Purely inflammatory dilatations will be 
referred to below. 

CIRCULATORY DISTURBANCES. 

Active hyperemia of the mucous membrane may be a part 
of acute inflammations of the tubes, and is very frequently found 
at the fimbriated extremity in association with peritonitis. The 
mucous membrane is swollen and bright red in color. There may 
be excess of mucous secretion. 

Passive hyperemia occurs in conditions in which the gen- 
eral venous circulation in the abdomen is impeded. 

Hemorrhages into the tubes may occur physiologically during 
the menstrual period, and sometimes considerable amounts of blood 
are found under these circumstances. Small hemorrhages into 
mucous membranes may occur in association w T ith inflammations 
of the tubes and in the course of some of the infectious diseases. 

Hematoma of the tube, or the collection of blood in the 
tube, results from stenosis of the lower end with accumulation 



664 



TEXT-BOOK OF PATHOLOGY. 



of the menstrual discharges in the proximal portions. The blood 
may remain in a more or less natural condition for a long time, 
or may undergo secondary changes. Sometimes it discharges 
through the abdominal end of the tube into the peritoneal 
cavity, and leads to retro-uterine hematocele. 

INFLAMMATIONS. 

Inflammation of the tubes, or salpingitis, may be acute or 
chronic. 

Acute salpingitis presents itself in several forms, such as an 
acute catarrhal and a suppurative form. In most cases the inflam- 




Fig. 323.— Acute septic salpingitis : section about the middle of the tube (Beyea). 



mation results from the entrance of irritants from the uterus, and 
the tubal disease is secondary, therefore, to endometritis or to other 



DISEASES OF THE REPRODUCTIVE ORGANS. 



665 



disease of the uterus. Among the micro-organisms discovered, 
streptococci, staphylococci, the gonococcus, the Diplococcus pneu- 
monia?, and the Bacillus coli communis may be mentioned. The 
infective organisms may extend directly along the mucous mem- 
brane, or more rarely may reach the tubes through the lymphatics. 
In rare instances salpingitis may be secondary to local peritonitis. 

Pathologic Anatomy. — In acute catarrhal salpingitis the mucous 
membrane is swollen, hyperemic, iniiltrated with round cells, and 
covered with more or less abundant mucous secretion, which may 
distend the tube considerably. In the later stages the secretion is 




Fig. 324.— Chronic salpingitis : both Fallopian tubes are closed and adherent (Penrose). 

apt to become mucopurulent. Interstitial inflammation, with 
thickening of all of the layers of the tube-wall, is frequently a 
secondary result. In acute suppurative salpingitis the walls of 
the tube are infiltrated with round cells (Fig. 323), the mucous 
surface may discharge abundant pus, and the tubes may become 
distended with this exudate if the abdominal and uterine ends are 
closed by the inflammatory process. This result, however, is less 
frequent than in the case of chronic salpingitis. The mucous 
membrane in these cases is intensely inflamed and often slightly 
ulcerated upon the surface. Sometimes the distention is so great 
that the tubes are converted into pus-sacs the size of an egg or a 
small lemon. In case of acute suppurative or necrotic salpingitis 
secondary to puerperal sepsis the mucous membrane may be covered 
with a necrotic membrane; the term diphtheritic salpingitis has 
sometimes been applied to such a condition. 

The exudates within the tube may remain for a long time with- 
out change, or may undergo gradual inspissation, and sometimes 



666 



TEXT-BOOK OF PATHOLOGY. 



even calcification occurs. When ulcers of the mucous membranes 
have formed, rupture of the tube and consecutive peritonitis may 
occur, especially during straining efforts, as in labor. Acute local 
or general peritonitis more frequently results from discharge of 
infective matter from the abdominal end of the tube. 

Microscopically, in all forms of salpingitis extensive round-cell 
infiltration is observed in all of the layers of the tubes. 

Chronic salpingitis, as a rule, results from the continuation 
of an acute form. The wall of the tube becomes thickened and 
the muscular layer is often hyperplastic. Proliferative changes in 
the mucous membrane are not unusual, and may lead to actual 
polypoid outgrowths. Occasionally small follicular formations 
are seen in the mucosa ; but ulcerations of the mucous membrane 
are infrequent. When the inflammation extends to the serous coat 
inflammatory adhesions are frequently formed (Fig. 324), and may 
bind the tube firmly to adjacent parts and occasion great conges- 




Fig. 325.— Hydrosalpinx, showing complete inversion of the fimbriae (Penrose ). 

tion or distortion. Very often the abdominal end of the tube be- 
comes occluded by inflammatory adhesions, or by inversion and 
agglutination of the fimbriae. At the same time the swelling of 
the mucosa obstructs the uterine end, and in consequence the tube 
becomes a closed pouch which fills with pus (pyosalpinx), sero- 
purulent liquid (hydrosalpinx) (Fig. 325), or hemorrhagic fluid 
(hematosalpinx). Intercurrent acute salpingitis frequently takes 
place in cases of chronic tubal disease. 

INFECTIOUS DISEASES. 

Tuberculosis of the tubes may be either primary or second- 
ary, and is probably much more frequent than has been supposed. 
Secondary tuberculosis may occur in the miliary form in associa- 
tion with tuberculosis of the peritoneum or with general tubercu- 



DISEASES OF THE REPRODUCTIVE ORGANS. 667 



losis. In other cases secondary tuberculosis leads to caseous and 
fibrous changes in the walls of the tubes. The latter become 
greatly thickened, and microscopically there is found a diffuse 
cellular infiltration with scattered giant cells and here and there 
definite tubercles. The fibrous changes progress more slowly, 
and may eventually become the conspicuous feature. Primary 
tuberculous salpingitis is similar in its appearance to the form 
just described. The infection may occur through entrance of the 
organisms at the uterine end of the tube, and certain observations 
would indicate that pre-existing gonorrheal salpingitis predisposes 
to secondary tuberculous infection. There are usually considerable 
adhesions of the tubes to the neighboring organs, and particularly 
to the ovary, and secondary miliary tuberculosis of the peritoneum 




Fig. 326. — Tuberculosis of the Fallopian tubes. The disease has extended to the perito- 
neum, which is covered with tubercles (Penrose). 

is frequently observed (Fig. 326). The lumen of the tube is filled 
with purulent liquid, and sometimes certain portions, particularly 
the abdominal end, may be greatly distended, forming cysts con- 
taining puriform liquid. 

Syphilis has been observed in the form of gummata, and also 
in the form of diffuse sclerosis, in cases of congenital origin. 

TUMORS. 

Fibromata and fibromyomata are met with in the external 
walls of the tubes as nodular masses. They frequently undergo 
secondary calcification. I4poma occurs in the external coat 
lying between the layers of the broad ligament. 

Papillomatous elevations of the mucous membrane are 
quite frequent, and in some cases a transformation of papilloma 
to carcinoma takes place. Probably most instances of primary 



668 



TEXT-BOOK OF PATHOLOGY. 



carcinoma of the Fallopian tubes have this origin. Secondary 
carcinoma may result from extension of uterine cancer. 

Sarcoma occurs in various forms, and Syncytioma ttialig- 

num may affect the tubes after tubal pregnancy. 

Cysts of the tubes are usually the result of localized distentions 
of the lumen in consequence of obstructions. Small cystic for- 
mations of obscure origin are sometimes found in the peritoneal 
covering of the tubes and along the attachment of the broad liga- 
ment. Their contents may be colloid or serous. 

The hydatids of Morgagni are small cystic formations about 
the size of a pea, hanging by a long pedicle at the fimbriated end 
of the tube. They are probably the result of distention of the 
closed end of Mtiller's canal. 

Tubo-ovarian cysts are formed by distention of the abdominal 
end of the tubes Avhen the fimbriated extremities are attached to 
the ovary, or in other cases may be the result of rupture of fol- 
licular cysts of the ovaries themselves into the abdominal end of 
the tubes. 

EXTRAUTERINE PREGNANCY. 

Ktiology. — Any obstruction to the downward migration of the 
ovum may lead to its retention and development in abnormal 
situations. The actual cause is usually difficult to determine. 
Impregnation possibly frequently takes place in the Fallopian 
tube ; but unless some obstruction arrests the passage of the ovum 
into the uterus, normal uterine gestation takes place. Swelling or 
rapid decidua-formation of the mucosa of the tubes may be one 
of the causes, and chronic salpingitis, by causing destruction of 
the cilia of the epithelial cells, and thickening and adhesions of 
the walls of the tubes, acts in a similar manner. Any other form 
of obstruction, as by tumors or external compression, may be 
included among the etiologic factors. 

Varieties and Pathologic Anatomy. — All cases of extra- 
uterine pregnancy are probably in the beginning tubal pregnancies. 
This condition may occur in any part of the tube. It is rarely 
found at the uterine end, but may occur there in that part of the 
tube which is embedded in the wall of the uterus. The term in- 
terstitial pregnancy is applied to this form. 

Tubal Pregnancy. — The changes which occur in the tube are 
analogous to those met with in the uterus. The same forms of 
membranes and decidual are developed, and a placenta develops, 
as in the uterus. The muscularis of the tube may hypertrophy 
somewhat; but in the end the increasing size of the contained 
ovum leads to thinning and stretching of the walls of the tube. 
It is an interesting fact that the mucous membrane of the uterus 
forms a decidua of more or less complete development in cases of 
extra-uterine pregnancy (Fig. 327). 



DISEASES OF THE REPRODUCTIVE ORGANS. 



669 



Among the terminations of tubal pregnancy are the following : 
1. The tube may rupture into the broad ligament, into the 
peritoneal cavity, or, in cases of interstitial pregnancy, into the 
uterus. As a result of these accidents hematoma of the broad 
ligament, hematocele, and local or general peritonitis may occur, 

.GHOftlO/M l<J VILLI 




Fig. 327.— Tubal pregnancy, removed before rupture. The opening that has been cut in 
the tube shows the chorionic villi (Penrose). 

or sudden death may take place as a direct result of the hemor- 
rhage. Sudden death from collapse is more frequently due to 
this cause than has generally been supposed. 

2. The ovum may be destroyed in the tube and the gestation 
cease. In this case the fetus subsequently undergoes various 
changes. More or less degeneration usually occurs, and shapeless 
masses or adipocere may result. In other cases calcification of the 
remnants of the disorganized fetus leads to the formation of a 
lithopedion. This may take place within the tube, or after rupture 
of the tube and enclosure of the fetus in a sac formed by circum- 
scribing peritonitis. 

3. Premature discharge of the ovum (tubal abortion) may occur, 
and the gestation may terminate without serious results. In other 
cases, however, it leads to a discharge of the blood through the 
unclosed abdominal ostium of the tube into the peritoneal cavity ; 
and hematocele, peritonitis, or sudden death from hemorrhage may 
occur. 

4. In very exceptional cases tubal pregnancy goes on to full 
term without rupture of the tube. Spurious labor may then 



670 



TEXT-BOOK OF PATHOLOGY. 



come on, the fetus, as a rule, perishing. The liquor amnii is 
absorbed, and degenerative changes leading to mummification, or 
the formation of adipocere or of a lithopedion, take place. The 
mummified fetus may remain for many years. Very rarely after 
spurious labor the fetus is discharged into the peritoneal cavity, 
and may be delivered through the rectum or in other ways. 

Abdominal Pregnancy. — This term is given to cases in which 
the tube has ruptured and the ovum, enclosed in its membranes, 
escapes into some part of the abdominal cavity, where it remains 
free or surrounded by adhesions the result of peritonitis. The 
placenta, as a rule, remains in the tube ; but it may also establish 
secondary attachments to parts of the peritoneum. Primary 
abdominal pregnancy — that is, impregnation and gestation in the 
abdominal cavity — does not seem ever to occur. 

THE VAGINA. 

PROLAPSE OF THE VAGINAL WALLS. 

Prolapse of the anterior or posterior wall of the vagina may be 
due to abnormal relaxation of the tissues, or it may be secondary 
to prolapse of the uterus and similar conditions that press the 
vaginal walls downward. Not infrequently the posterior wall of 
the bladder is dragged downward with the anterior wall of the 
vagina, and vaginal cystocele results. Similarly the anterior wall 
of the rectum may be carried downward with the posterior wall 
of the vagina ; this is termed vaginal rectocele. 

STENOSIS OF THE VAGINA. 

Congenital stenosis is rare. More frequently the lumen of the 
vagina is narrowed by contraction of cicatricial tissues formed in 
inflammatory diseases of the walls, or by adhesion of the opposite 
surfaces following ulcerations. Complete occlusion may occur in 
the latter form of cases, especially in old women. 

WOUNDS AND FISTUL/E. 

Injuries to the vaginal walls may be caused by the insertion 
of sharp bodies or instruments, or by coitus. Much more fre- 
quently injuries are due to stretching or pressure during labor. 
Superficial lacerations caused by overdistention are frequent, but 
more extensive injuries may be caused by prolonged pressure of 
the infant's head or by instruments used in delivery. In such 
cases infection and phlegmonous inflammation are prone to occur, 
and vesico-vaginal, urethro-vaginal, or recto-vaginal fistulse are 
sometimes the result. The urine or feces may be discharged 



DISEASES OF THE REPRODUCTIVE ORGANS. 671 



through the vagina, and often cause secondary inflammations of 
the entire vaginal mucosa. 

Similar fistulse may be due to ulcerative processes of other . 
kinds, to necrosis of carcinomata of the vagina, or to diseases of 
the bladder or rectum. 

CIRCULATORY DISTURBANCES. 

Active hyperemia occurs in the early stages of inflamma- 
tion. The mucous membrane is light red in color and a little 
swollen. 

Passive hyperemia is frequent in pregnancy ; and occurs in 
consequence of pressure due to other causes, such as uterine 
tumors and the like. The mucosa becomes swollen and edema- 
tous, and may be moist from increased secretions. 

Hemorrhages into the vaginal walls are most frequently due 
to traumatism. Inflammation and ulceration may result from the 
hemorrhagic extravasation. 

INFLAMMATIONS. 

Acute Catarrhal Inflammation, Vaginitis, or Colpitis. 

— This condition is frequently due to gonorrheal infection, but 
may result from other causes, such as mechanical and chemical 
irritants, or in young girls from the invasion of the Oxyuris 
vermicularis from the rectum. The mucous membrane is usu- 
ally deeply congested, and the surface is covered with muco- 
purulent exudate. In gonorrheal cases the cervix uteri and 
urethra are, as a rule, coincidently affected. 

Exfoliative Vaginitis. — In rare cases of intense catarrhal 
vaginitis, in which the deeper layers of the mucosa are principally 
involved, membranous formations, consisting of parts of the super- 
ficial epithelial layers, may be discharged. 

Pseudomembranous vaginitis may occur in association 
with various infectious diseases, such as pneumonia, pyemia, 
cholera, etc. ; but it is more frequently the result of pressure- 
necrosis and infection occurring during labor, and is one of the 
lesions of puerperal sepsis. The surface of the vagina is more or 
less extensively covered with a dirty and exfoliating pseudomem- 
brane. After discharge of the latter ulcerations are often formed. 
Extensive necrosis of the vaginal walls may occasion great de- 
struction, and in some instances phlegmonous inflammations of 
the perivaginal tissues may cause separation of the mucosa. 

Chronic catarrhal vaginitis may be the continuation of an 
acute inflammation, or may occur in a gradual manner in women 
reduced in vitality. The mucosa usually presents appearances 
somewhat like those of acute cases, though the congestion is less 



672 



TEXT-BOOK OF PATHOLOGY. 



marked. Abundant mucopurulent or mucous discharge (leucor- 
rhea) may be present. Erosions of superficial epithelium and 
enlargements of the lymphoid follicles are sometimes observed. 
In long-standing cases the surface may be smooth and the entire 
mucosa somewhat indurated. 

INFECTIOUS DISEASES. 

Tuberculosis may occur in the form of ulcers associated with 
uterine tuberculosis, or in the form of lupus from extension of 
the latter from the vulva. 

Syphilis. — Chancres may occur in any part of the vagina, 
and circumscribed (gummatous) or diffuse infiltrations have been 
described. 

TUMORS. 

Fibroma and myofibroma may arise in the muscular layer 
of the vaginal wall, and may project as nodular masses or assume 
a polypoid form. 

Sarcoma may occur as a circumscribed mass, but more com- 
monly as diffuse infiltration which tends to ulcerate. 

Papillomata are not infrequent, in the form of small warts 
or as considerably elevated condylomata. 

Carcinoma of the vagina is most frequently secondary to 
cervical cancer. Similarly it may follow cancer of the vulva. 
Primary carcinoma of the vagina is rare. It occurs in the form 
of a circumscribed villous projection. 

Cysts of the vaginal walls vary in size and number. Fre- 
quently they are multiple, and the size ranges from scarcely dis- 
coverable cavities to those the size of an egg. The contents are 
usually serous and colorless, or less frequently of brownish color. 
In some instances a flat epithelial lining has been discovered. 
The origin of these cysts is probably variable. Some seem to 
arise from remnants of the lower end of the Wolffian duct; 
others are probably lymphangiectatic. The multiple small cysts 
sometimes occurring in pregnancy are due to follicular distentions, 
or to small hemorrhages with subsequent cystic change. 

THE DECIDUA, PLACENTA, AND FETAL MEMBRANES. 

Anatomic Considerations. — The fetus is enclosed within 
a delicate fibrous membrane, the amnion, and this is covered with 
a second membrane, the chorion. After the deposit of the ovum 
in the uterus the mucous membrane of the latter undergoes a form 
of hyperplasia, in which the uterine glands and the blood-vessels 
take part conspicuously, and thus the organ becomes lined with a 
thickened mucosa. The latter is termed the decidua vera. A 



DISEASES OF THE REPRODUCTIVE ORGANS. 673 



reflection from this covers the fetus enclosed in its membranes, 
the reflection being known as the deeidua reflexa. At about the 
fifth month of development the deeidua reflexa and the deeidua 
vera unite and fuse. The portion of the deeidua vera at which 
the placenta is subsequently located is termed the deeidua serotina. 
In this portion the vascular system is particularly marked, and is 
composed of large venous sinuses with thin walls. The fetal cho- 
rion carries on its outer surface numerous small projections, or 
villi. In the region of the deeidua serotina these villi undergo 
marked hyperplasia and bury themselves between the venous 
sinuses of the deeidua. At the junction of the villi and the 
deeidua two layers of cells are developed. The first, immediately 
covering the villi, consists of cubical epithelial cells (Langhan's 
cells). Outside of these, and uniting the villi with the maternal 
tissue, is a layer of clear protoplasmic material containing large 
nuclei. This has the appearance of nucleated protoplasm, rather 
than that of collections of cells of definite outline. This proto- 
plasmic layer, syncytium, is probably, like Langhan's cells, derived 
from the covering of the chorionic villi though some authorities 
contend that it is maternal in origin. 

ABNORMALITIES OF DEVELOPMENT. 

The Placenta. — Abnormal smallness of the placenta, or 
hypoplasia, and abnormal largeness are occasionally observed. 
More frequently an adventitious placenta (placenta succenturiata) 
may be attached to the main placenta, or may lie near it. Abnor- 
mal location of the placenta at or near the neck of the uterus 
(placenta prcevia) is an important condition, from its liability to 
cause hemorrhage and miscarriage. 

The Umbilical Cord.— Occasionally the cord is divided near 
its placental end into two or more branches. The placenta may 
be correspondingly divided, or single. The attachment to the 
placenta may be marginal instead of central, and sometimes the 
blood-vessels spread out into a broad marginal attachment, with 
absence of their gelatinous covering. The latter is termed vela- 
mentous insertion. 

Abnormalities of the blood-vessels, such as branching, a single 
artery, two veins, etc., are unimportant. 

Twists and knots of the cord are frequent, and may strangulate 
the cord and stop the circulation, causing death of the fetus. 

Thickening of the intima of the umbilical vein and of the ad- 
ventitia of the arteries is probably syphilitic in nature. 

CIRCULATORY DISTURBANCES. 

Hydrorrhea gravidarum is a condition in which abundant 
serous or somewhat turbid liquid is secreted from the deeidua?. 

43 



674 



TEXT-BOOK OF PATHOLOGY. 



The condition occurs in women suffering from general anemia, but 
is probably due to local conditions within the uterus. Abortion or 
miscarriage is not unusual. 

Hemorrhages from the decidua or into the decidua and pla- 
centa are not infrequent. Hemorrhages from the surface may be 
due to preceding decidual disease, or may be obscure in origin. 
Large hemorrhages may cause rapid discharge of the uterine con- 
tents. In cases of that abnormal position of the placenta called 
placenta praevia hemorrhages are frequent. 

Fleshy moles is the term used to designate formations in the 
decidual and placenta resulting from gradual hemorrhage and 
destruction of the ovum. The hemorrhage takes place in the 
decidua, and then extends between the chorionic villi into the fetal 
membranes, which may be more or less extensively torn apart. 
Irregular masses of clotted blood attached to the placental site and 
to the chorion are discovered. The amniotic cavity contains vis- 
cid fluid and the ovum is more or less completely disorganized. 
Sometimes no recognizable remnants can be found. The moles 
may be retained a long time, and may undergo secondary calca- 
reous infiltration. Usually they are soon discharged. 

Placental Infarcts.— This term is applied to light-colored, 
more or less indurated areas met with in the placenta, decidua?, 
and sometimes in the chorion. The nature of these formations is 
still somewhat uncertain. They are composed of fibrin, of reticu- 
lated or granular character, with occasional areas of softening and 
hemorrhagic accumulations, and are not rarely surrounded by a zone 
of cellular infiltration. Some of these " white infarcts " may be 
only an exaggeration of the normal coagulation-necrosis occurring 
toward the end of pregnancy. When they are extensive it is very 
probable that they represent results of disturbances of circulation 
caused by thickening of the walls of the blood-vessels. 

INFLAMMATION. 

Inflammations of the placenta {placentitis), of the chorion villi, 
or of the decidua (endometritis decidual is) may occur in association 
with preceding diseases of the uterus, and especially in cases of 
svphilis of the mother or fetus. The inflammation takes the form 
of cellular infiltration and induration. This may begin in the 
decidua and extend to the placenta, and may be of a diffuse or 
circumscribed character. The villi of the placenta may be greatly 
compressed by the inflammatory tissue, and may suffer fatty de- 
generation and atrophy. In other cases the inflammatory changes 
are most pronounced in the walls of the blood-vessels and around 
the vessels of the chorion and umbilical cord. Nodular thickening 
or diffuse induration results, the latter especially in cases in which 
coincident involvement of the chorionic villi has occurred. 



DISEASES OF THE REPRODUCTIVE ORGANS. 



675 



Diffuse hyperplasia of the decidua is sometimes described as 
endometritis decidualis. The inflammatory nature of such cases, 
however, is uncertain. 

INFECTIOUS DISEASES. 

Tuberculosis of the placenta was suspected as a possible con- 
dition long before positive demonstrations were made. In recent 
years, however, a number of undoubted cases have been described. 
Macroscopically there may be but little change in the appearance 
of the affected parts. 

Small tubercles, containing abundant giant cells and tubercle 
bacilli, first appear in the decidua serotina, and later invade the 
placental and chorionic tissues between the villi. The epithelial 
covering of the villi undergoes hyperplasia, forming collections of 
large cells. In the later stages of the process caseous necrosis of 
the tubercular structures takes place, and the villi themselves suf- 
fer invasion and degeneration. Their blood-vessels are frequently 
occluded by hyaline thrombosis and proliferation of the endothelial 
lining. Tubercle bacilli have been demonstrated in the vessels of 
the fetal side of the placenta, though less frequently and abund- 
antly than in the maternal vessels. 

Syphilis of the placenta may take the form of a diffuse hyper- 
plasia, or of a nodular or gummatous process. The placenta is 
enlarged, indurated, and heavy ; it is light colored in localized 
areas or diffusely. Microscopically, cellular proliferation spring- 
ing from the adventitia of the blood-vessels is the characteristic 
feature. The epithelial cells covering the villi may proliferate, 
and fatty degeneration of the body of the villi is not infrequent. 
The chorion and amnion may be diffusely thickened. The syphi- 
litic nature of cases conforming with the above description is often 
doubtful, as is also the nature of some of the cases of placentitis 
that are often described as syphilitic. 

HYPERPLASIA. 

Occasionally diffuse or circumscribed thickening of the decidual 
occurs in association with chronic metritis ; the term endometritis 
decidualis is applied to this condition (see Inflammation). 

Placental Polyps. — Portions of the decidua, and especially 
the placenta, retained in the uterus, may remain firmly attached 
and may undergo subsequent proliferative change, forming poly- 
poid tumors of adenomatous structure. These are particularly 
frequent after abortion. 

Destructive Placental Polyps. — Like the preceding, these 
originate in retained portions of the placenta, but differ in the 
more active proliferative changes that take place. On the uterine 
surface they are covered with fibrin and blood-clots, and at their 



676 



TEXT-BOOK OF PATHOLOGY. 



attachments are composed of variously formed cells, including 
large epithelium-like cells enclosed in a vascular stroma. The 
growth may involve the uterine tissues to a considerable extent. 
Its nature is obscure in some particulars, but resembles that of the 
syncytioma. 

Hydatid moles present themselves as rounded, rather trans- 
lucent bodies hanging by their pedicles to the outer surface of the 
chorion, and often attached one to another in clusters, resembling 
a bunch of grapes. Microscopically they are found to be composed 
of myxomatous or more or less edematous fibrous tissue containing 
few cells and free nuclei, and covered in the outer surface by epi- 
thelial cells (Fig. 328). The nature of the hydatid mole has been 




Fig. 328.— Section of a hydatid mole. 



the subject of some controversy, Virchow taught that they are 
simply myxomatous hypertrophied chorionic villi. More recent 
investigators have found evidences of active hyperplasia of the 
superficial epithelium of the chorion villi, with secondary degen- 
eration, edema, and necrosis. This accounts for the fact that 
sometimes the moles extend deeply into the decidua, and even 
into or through the muscular wall of the uterus. 

Hydatid moles are especially met with in women suffering from 
chronic constitutional diseases (nephritis, anemia) and in those be- 
coming pregnant late in life. Endometritis seems to bear some 
relation, though the disease is evidently one of the fetal rather 
than maternal tissues. This is shown by the limited extent of the 
disease in some cases, and by the fact that in twin pregnancy the 
membranes of only one of the fetuses may be affected. When the 
disease is extensive death of the fetus usually results, and the 



DISEASES OF THE REPRODUCTIVE ORGANS. 677 

moles are discharged in the form above described, or enclosed in 
clotted blood. 

Syncytioma Malignum. — The nature and peculiarities of 
this condition have been sufficiently described (see page 162). 



THE VULVA. 
WOUNDS. 

Injuries of the vulva frequently occur during labor. Lacera- 
tion of the fourchette is very common, and in a considerable pro- 
portion of cases more extensive tears extending into the perineal 
body, and sometimes through this into the rectum, are observed. 
Prolonged pressure and contusion during labor may occasion 
hemorrhages into the tissues of the vulva. 

CIRCULATORY DISTURBANCES. 

Active hyperemia is met with in acute inflammations. 

Passive hyperemia and edema occur in conditions in which 
there is general venous stasis, as in cardiac or pulmonary diseases. 
They are also met with in pregnancy. The vulva is dark red in 
color, sometimes cyanotic ; the subcutaneous and submucous tis- 
sues become edematous, and in consequence the labia majora may 
swell enormously. 

Hematoma of the vulva is caused by compression and contu- 
sion of the vulva during parturition, or less frequently at other 
times. Varicosity of the veins is a predisposing cause of import- 
ance. Considerable masses of blood (" thrombi ") accumulate in 
the submucous tissues of the vulva and vagina. These may be 
subsequently absorbed, or they may discharge through the skin in 
consequence of superficial ulcerations and ruptures. Infection of 
the thrombus may cause abscess of the labia or other affected 
parts. 

INFLAMMATION. 

Acute catarrhal inflammation results from the same causes 
as occasion acute vaginitis. The pathologic appearances are, in 
general, the same, though edematous swelling is likely to be more 
marked. Distention of the glands of Bartholin and secondary 
abscess-formation in these glands are common conditions in 
gonorrheal vulvitis. 

Chronic inflammation sometimes follows acute vulvitis. 
Considerable hyperplasia of the mucosa is sometimes the result. 
Erosions and ulcerations are less frequent. 

Phlegmonous inflammation, or abscess, of the sub- 
mucous tissue of the labia majora sometimes results from exten- 



678 



TEXT-BOOK OF PATHOLOGY. 



sion of a similar process in the adjacent parts, or may be the 
direct result of injuries and hematoma, with secondary infection. 

INFECTIOUS DISEASES. 

Diphtheria sometimes attacks the vulva, especially in puer- 
peral women. The pathologic conditions are similar to those 
observed in other mucous membranes. 

Tuberculosis may occur in the form of lupus. The lesions 
are irregular ulcers with elevated edges and more or less necrotic 
bases. 

Syphilis. — Chancres are met with on the sides of the labia 
and elsewhere. 

Chancroids occur in the same situations as chancres. Very 
often opposite sides of the vulva are involved by attrition. 

Gangrene of the vulva may be the consequence of severe 
contusions or inflammations occurring in the course of various 
infectious diseases. 

TUMORS. 

Fibroma, fibromyxoma, and myofibroma are occasion- 
ally met with as nodular tumors or polyps arising from the labia 
majora. I/ipoma and sarcoma may present a similar macro- 
scopic appearance. All of these growths are rare. 

Elephantiasis vulvae is a not infrequent affection, especially 
in eastern and tropical countries. It may be due to congenital 
dilatations of the lymphatic channels, or to lymphangiomatous 
tumor-growths. More frequently elephantiasis is caused by 
inflammatory conditions that occasion obstruction to the flow of 
the lymph. In some instances the etiology is very obscure. 

Pathologically, elephantiasis consists of a thickening of the 
subcutaneous connective tissue, with more or less involvement of 
the skin as well. The disease may begin in the clitoris, or in one 
or other of the labia, and may be confined to the part primarily 
affected, or may extend to other parts. The affected portions are 
tough and edematous ; the skin is tightly bound to the subcuta- 
neous tissue. The surface may be irregularly elevated, but in 
other cases is smooth. Superficial ulcers may occur, and some- 
times the dilated lymph-channels communicate with the surface, 
discharging lymph (lymphorrhea). 

Papillomatous tumors are not infrequent in syphilitic 
women in the form of elevated condylomata. A somewhat 
analogous condition of obscure etiology is that termed caruncle. 
It presents itself as a papillomatous and highly vascular elevation 
at the meatus of the urethra. 

Adenoma arising from the glands of Bartholin has been 
described. 



DISEASES OF THE REPRODUCTIVE ORGANS. 679 



Carcinoma is uncommon. It most frequently arises from the 
clitoris, but may affect any portion. Glandular cancer may begin 
in Bartholin's glands. 

Cysts are quite frequent. Small retention-cysts, containing 
pultaceous (atheromatous) matter, are sometimes met with in the 
labia majora. Larger cysts, containing serous or somewhat blood- 
stained liquid, may result from hematomata, or may be lymphan- 
giomatous in origin. Hydrocele of the canal of Nuck has the 
superficial appearances of a cyst of the labia. Retention-cysts of 
Bartholin's glands have been referred to above. 

THE PENIS AND SCROTUM. 

CONGENITAL ABNORMALITIES. 

Absence of the penis is rarely observed ; more frequently it is 
abnormally small, resembling the clitoris of the female. Occasion- 
ally the organ is doubled, each half containing a duct, one for the 
discharge of urine, the other for seminal fluid. 

Hypospadias is the condition in which the urethra terminates 
in an orifice on the under surface of the penis, in the pendulous 
portion or at the bulb, or occasionally at the root of the scrotum 
or in the perineum. Epispadias is a less frequent condition ; the 
urethral orifice in this case is found upon the dorsal side of the 
organ. Excessive length of the prepuce is a frequent abnormality ; 
there may be associated with this stenosis of the preputial opening, 
so that the glans penis cannot be exposed (phimosis). 

INFLAMMATION. 

Inflammation of the mucous membrane of the glans 
penis (balanitis) and of the prepuce (posthitis) is not infrequent. 
Among the more frequent causes are uncleanliness, with decompo- 
sition of smegma retained beneath the prepuce, irritation by the 
urine in cystitis or other inflammatory diseases, gonorrheal infec- 
tion, and chancroids. The mucous membrane becomes swollen 
and red, and considerable purulent exudate may be discharged. 
Edematous swelling of the prepuce is frequent, and may cause 
inability to retract the prepuce over the glans (phimosis). In other 
cases the prepuce, previously drawn back, becomes so tensely 
swollen that it cannot be pushed forward to its normal position 
( pai'aphimosis). 

In catarrhal inflammation of the prepuce there may be associ- 
ated retention-cysts of the mucous glands. The cysts may rupture, 
causing small ulcerations. 

Inflammation of the cavernous bodies may result from 
traumatism, or from extension of gonorrheal urethritis, and may 
sometimes occur in infectious diseases, such as small-pox, pyemia, 



680 



TEXT-BOOK OF PATHOLOGY. 



etc. The penis swells considerably, and abscesses or diffuse puru- 
lent infiltration may result. In traumatic cases with hemorrhagic 
exudation necrosis or gangrene may result. In case of favorable 
termination after severe inflammations cicatrices may be formed. 

INFECTIOUS DISEASES. 

Syphilitic chancres and soft chancre or chancroid are 

frequently located upon the prepuce or its frenum, or upon the 
glans penis (the lesions are described in Part I.). 

Tuberculosis is a rare condition in this situation. It has 
been met with in the form of necrotic ulcerations. It is very 
likely that direct infection of the penis may occur during coitus 
with a woman who has genital tuberculosis. 

TUMORS. 

Papilloma, or condyloma acuminatum, is not infrequent 
on the glans penis and prepuce. Sometimes it has a distinctly 
inflammatory origin, occurring in association with gonorrhea, 
syphilis, or other forms of local irritation ; in other cases it origi- 
nates without discoverable cause. There are usually several or 
many warty elevations, and occasionally a mass of warts is 
aggregated in a cauliflower fashion. Microscopically, condy- 
lomata are composed of a stroma of vascular connective tissue 
covered with squamous epithelium. The cauliflower-form may be 
distinguished from epithelioma by observing that the mucous mem- 
brane is not infiltrated and is movable upon the underlying tissues. 

Carcinoma (epithelioma) of the penis may arise from the 
glans or from the prepuce. It may present itself as an infiltrating 
growth with a tendency to ulceration, or as a papillomatous, cauli- 
flower-like growth. In the latter case it is probable that the pri- 
mary growth was papillomatous;, with secondary carcinomatous 
association, or that the original tumor was carcinomatous, followed 
by papillomatous outgrowths. Considerable destruction of the 
glans penis may occur, and metastatic nodules are frequently 
formed in the inguinal glands. 

Epithelioma of the scrotum is comparatively frequent in chim- 
ney-sweeps and paraffin-workers. 

Elephantiasis of the scrotum is a common disease of the 
East. The scrotum may be enormously enlarged. Some cases 
are due to filariasis ; in other cases filariaB cannot be demonstrated. 
Somewhat similar thickening of the prepuce is a rare condition. 

Cysts. — Small cysts, due to occlusion of the glands of the 
mucous membrane and of the skin, are occasionally met with un- 
der the prepuce and in the scrotum. Dermoid cysts of the scrotum 
are occasionally observed. 



DISEASES OF THE REPRODUCTIVE ORGANS. 681 



I4pomata, angiomata, and fibromata are rare forms of 
tumors of the penis. 

Concretions beneath the prepuce result from phimosis with 
retention of the smegma. Sometimes they increase by constant 
additions until they reach considerable size (200 g.). In one case 
under my observation gouty tophi in the prepuce grew to the size 
of a small lemon. 

INJURIES OF THE PENIS. 

Direct traumatism may occasion serious laceration of the cor- 
pora cavernosa, especially when the penis is erect at the time of 
injury. Considerable hemorrhagic extravasation may occur, and 
inflammation or even necrosis and gangrene may ensue. Fracture 
of the penis is a term applied to rupture of the fibrous capsule of 
the cavernous bodies. Both this and less extensive lacerations 
occasion great hemorrhagic swelling, with subsequent inflamma- 
tion or necrosis. Injuries to the penis may cause rupture of the 
urethra, with extravasation of urine. 

THE TESTICLES. 

CONGENITAL ABNORMALITIES. 

Absence of one or both testicles is a rare condition. More fre- 
quently the organ is hypoplastic, remaining undeveloped through 
life. 

The most frequent congenital abnormality is eryptorehismus, 
the condition in which one or both testicles remain in the abdomi- 
nal cavity, in the inguinal canal, or elsewhere in the tract through 
which normal descent occurs. The undescended testicle may de- 
scend at or before puberty, or may remain fixed in its abnormal 
position. In the latter case, especially if the testicle is in the 
inguinal canal, secondary inflammation or atrophy may occur. 
Slight defects in the development of the testicle are not infre- 
quent, but are unimportant. 

ATROPHY AND HYPERTROPHY. 

Atrophy may follow any form of inflammation of the testicle 
or epididymis, such as those occurring after gonorrhea, mumps, 
and other infectious diseases or traumatism. In other instances 
pressure upon the organ, as in hydrocele, tumors, etc., is the cause 
of atrophy. The most frequent form is that which occurs as a 
natural process of involution in old age (senile atrophy). 

The testicle decreases in size, increases in hardness from over- 
growth of connective tissue, and is usually more pigmented than 
in health. Microscopically the seminal tubules are found to have 



682 



TEXT-BOOK OF PATHOLOGY. 



undergone fatty degeneration, and contain fatty debris and blood- 
corpuscles. 

Hypertrophy of one testicle may occur as a compensatory 
process in cases of disease, atrophy, or removal of its fellow. 
Hypertrophy of this sort has been produced experimentally in 
animals. The seminal tubules increase in size, but are otherwise 
normal. 

DEGENERATIONS. 

Fatty degeneration is frequently observed in testes sub- 
jected to pressure through tumors or other pathologic conditions, 
and in cases of atrophy of the testicle from any cause. The epi- 
thelium of the tubules is attacked, and may be completely de- 
stroyed, with production of fatty detritus. 

Myxomatous degeneration occurs in various tumors of the 
testis and in gummata. 

Calcification may affect old inflammatory deposits, especially 
those of the epididymis. 

Caseation is a frequent condition in tuberculous and syphilitic 
lesions ; and abscesses may undergo a process of inspissation, with 
formation of dry, caseous material. 

CIRCULATORY DISTURBANCES. 

Active hyperemia of the testis, epididymis, and especially 
of the membranes, occurs in association with acute inflammations. 

Passive hyperemia is caused by pressure upon the veins or 
disease of the veins (varicosity). The testis and epididymis be- 
come swollen from edema, and, if the hyperemia persists, fatty 
degeneration and atrophy may result. Serous effusion into the 
tunica vaginalis {hydrocele) may occur, but this condition is more 
frequently inflammatory (see page 684). 

Embolism of the spermatic artery may occasion hemorrhagic 
infarction, followed by necrosis or gangrene of the testis. This 
sequence has been observed in a few cases, and has been proved 
experimentally. Sometimes gangrene seems to be caused by 
phlebitis of the pampiniform plexus. 

INFLAMMATION. 

Inflammation may involve the testis (orchitis), the epididymis 
(epididymitis), or the tunica vaginalis (vaginitis testis). 

Etiology. — Traumatism is a frequent factor in the etiology, 
and causes inflammation of the epididymis and membranes more 
frequently than of the testicle itself. Blows, bruises, and contu- 
sions are the usual conditions that cause this form of inflammation. 

In another group of cases the irritants are micro-organisms 
conveyed through the blood. Thus in typhoid fever, tuberculosis, 



DISEASES OF THE REPRODUCTIVE ORGANS. 683 



pneumonia, and various forms of septicopyemia the specific organ- 
isms have been discovered in the areas of inflammation. Similar 
inflammations occur in mumps, scarlet fever, syphilis, and small- 
pox, and are doubtless caused in the same way, though the spe- 
cific organisms are unknown. In these cases the testis is more 
frequently affected than the epididymis. 

In a third group of cases infection occurs through the vas deferens, 
and the epididymis is affected first and often alone. The most 
frequent infectious agent in this group of cases is the gonococcus ; 
but other micro-organisms may enter the vas deferens, reach the 
epididymis and cause inflammation, in other diseases of the bladder 
or urethra, or after operations upon these parts, such as crushing 
vesical calculi, cutting urethral strictures, and the like. 

Pathologic Anatomy. — Inflammations of the different parts 
may be separately considered. 

Acute Orchitis. — In acute orchitis the testis is swollen and more 
or less edematous on account of inflammatory exudation. Micro- 
scopically the striking feature is round-cell infiltration of the 
intertubular tissues. This may be diffuse and uniform, or may 
occur in circumscribed areas. The latter is especially common in 
the orchitis of variola and pyemia. The round cells may infiltrate 
the walls of the tubules, and may be discharged into the tubules 
in great numbers. At the same time the epithelial cells may suffer 
degeneration and desquamation. Intense orchitis may lead to the 
formation of abscesses, single or multiple. These may subse- 
quently undergo complete absorption, or may become inspissated 
and encapsulated, the contents of such a focus consisting of fatty 
detritus and cholesterin. In other cases the abscess may rupture 
externally, and occasionally granulations springing from the tunica 
albuginea or the testis may protrude through the opening. The 
term benign fungus is applied to this condition. 

Chronic orchitis usually results from the acute form. The 
inflammatory changes of the intertubular tissues gradually lead to 
induration, and the testis becomes hard and contracted, the con- 
nective tissue and septa being increased in density, the tubules at 
the same time suffering degeneration and atrophy. In cases fol- 
lowing acute suppurative orchitis the tissues surrounding the 
inspissated abscess become sclerotic, and the tubules are in large 
part or wholly destroyed. Small nodular areas are discovered in 
such cases, and on section these are found to consist of a dense 
wall of fibrous tissue enclosing thickened pus containing fatty 
detritus and cholesterin. The membranes surrounding the testis 
are usually thickened and united by adhesions. 

Chronic orchitis without a definite antecedent acute stage is a 
frequent result of syphilis (see page 686). 

Acute epididymitis occurs when infective agents have reached 
the epididymis through the vas deferens. There is tense swelling 



684 



TEXT-BOOK OF PATHOLOGY. 



of the epididymis, and not rarely associated inflammation with 
serous exudation in the tunica vaginalis. The testis is not, as a 
rule, involved. The process begins as an acute catarrhal inflam- 
mation of the tubules of the epididymis ; later, cellular infiltra- 
tion and occasionally abscess-formation occur in the intertubular 
connective tissues. The inflammation is sometimes completely re- 
solved, but in other cases fibrous thickening, diffuse or nodular, 
results. Inspissated abscesses surrounded by fibrous tissue are 
sometimes seen, as in orchitis. The epithelium of the tubules 
embedded in the new-formed fibrous tissue may undergo a cer- 
tain amount of proliferation, suggesting the appearance of ade- 
noma or cancer. The vas deferens may be permanently ob- 
structed, and the tubules on the proximal side and in the testis 
may undergo cystic distention. Extensive epididymitis very 
commonly causes atrophy of the testis. 

Vaginitis testis and periorchitis are terms applied to inflamma- 
tion of the tunica vaginalis testis. This condition is usually the 
result of orchitis or epididymitis, but may sometimes occur as a 
primary inflammation resulting from traumatism or other forms of 
irritation. 

The tunica vaginalis is a reflection of the peritoneum, and in- 
flammatory conditions arising in it resemble those of the abdomi- 
nal peritoneum. 

Serous or serofibrinous vaginitis testis is the most frequent 
form. This may be acute or chronic, and is characterized by the 
accumulation of small or large collections of serous liquid. In 
slowly developed cases the quantity of liquid may be one or two 
liters. It may be clear serum, but often contains flakes of fibrin, 
or leukocytes, and is sometimes reddish from the presence of red 
blood-corpuscles. Sometimes the liquid is milky or turbid, and 
contains fat-droplets and cholesterin-crystals. A chylous variety 
occurs in tropical countries, and is probably caused by the Filaria 
sanguinis hominis. 

Hydrocele is the term used to designate effusions of these sorts. 
Sometimes the liquid contains spermatozoa, when the term hydro- 
cele spermatica is applied. This condition is due to the escape of 
spermatozoa from improperly developed spermatic tubules or from 
ruptured cysts of the epididymis or testis. In certain cases it is 
difficult to distinguish hydrocele sperm atica and spermatocele (see 
page 668). 

When hydrocele persists the tunica vaginalis undergoes hyper- 
plastic thickening, and small, wart-like elevations may be formed 
(periorchitis prolvfera). These nodules may become separated and 
remain in the sac as free bodies, like those in the joints. Another 
result of the secondary inflammatory changes in the membrane is 
adhesion of the reflexions, causing a bilocular or multilocular 
hydrocele. 



DISEASES OF THE REPRODUCTIVE ORGANS. 685 



When the canal connecting the sac with the peritoneal cavity 
has remained patulous the fluid of hydrocele may be pressed into 
the abdominal cavity. The term hydrocele processus vaginalis is 
applied to such cases, and the term hydrocele funiculi spermatid to 
cases in which only the upper part of the vaginal canal is patulous 
and filled with liquid. Hydrocele funiculi cystica results from col- 
lections of fluid in the middle portion of the canal, the upper and 
lower ends being obliterated. 

Purulent vaginitis testis occurs in association with epididy- 
mitis and orchitis, and sometimes primarily after traumatism. An 
ordinary hydrocele may be converted into a purulent collection by 
puncture with infected instruments. The sac is more or less dis- 
tended with purulent liquid, and the surface of the membrane is 
covered with fibrinopurulent exudate. The pus may discharge 
externally, or may become inspissated ; and extensive adhesions 
may obliterate the sac. 

Hemorrhagic Vaginitis Testis. — In severe acute inflammations 
the exudation may be more or less hemorrhagic. More distinctly 
hemorrhagic forms of inflammation result from traumatism ; in 
these cases there is first extravasation of blood and then inflamma- 
tion. The sac may be lined with fibrinous and hemorrhagic depos- 
its, and the membrane becomes thickened. In the terminal stages 
considerable thickening and sometimes calcification of the tunica 
vaginalis are observed. 

Inflammation of the vas deferens may be associated with 
epididymitis or orchitis, or may occur independently in cases of 
direct traumatism. In syphilitic disease of the testis, and less 
commonly in other forms of orchitis, the vas deferens may be 
greatly thickened. 

INFECTIOUS DISEASES. 

Tuberculosis is most frequent in the epididymis, but may 
involve the testicle as well. The infection occurs in one of two 
ways : either through the vas deferens, in consequence of tuber- 
culosis of the prostate, seminal vesicles, or bladder ; or through 
the circulation in cases of pulmonary or other forms of tubercu- 
losis. It has been shown that tubercle-bacilli are discharged from 
the body in the seminal fluid in cases of pulmonary and other 
forms of tuberculosis ; and when local conditions predispose tuber- 
culous infection of the epididymis may occur. Gonorrheal epidid- 
ymitis seems to constitute such a local predisposition. Primary 
hematogenous infection of the epididymis seems to occur in rare 
cases. 

In cases of infection through the vas deferens there are formed 
in the walls of the tubule of the epididymis small tubercular masses, 
which rapidly increase in size and run together, forming caseous 



686 TEXT-BOOK OF PATHOLOGY. 

areas of considerable size. Further invasion occurs along the 
lymphatic channels and the tubule, and rapid involvement of a 
considerable part of the epididymis results (Fig. 329). The tub- 
ule surrounded by tuberculous tissue may become filled with des- 




Fig. 329. — Tuberculosis of the epididymis and testicle (modified from Bollinger). 

quamated epithelium and puriform or caseous matter, and may be 
dilated in a cystic form. Extension to the testicle may occur, but 
is unusual. 

Associated serous or serofibrinous vaginitis testis is not infre- 
quent ; and in some cases the tuberculous disease itself extends to 
the testicular envelopes and causes nodular elevations, or ulcera- 
tions and fistulous communications with the surface. 

Hematogenous tuberculosis of the epididymis is, in the first 
place, of the miliary form ; but the tubercles grow rapidly and 
caseous nodules are rapidly formed. 

Tuberculosis of the vas deferens may be secondary to tubercu- 
losis of the seminal vesicles and bladder, or of the epididymis. 
It is characterized by caseous swelling of the Avails of the duct. 

Syphilis is not infrequently seen in the testicle in the late 
stages of acquired syphilis and in congenital syphilis. The epi- 
didymis and the membranes are secondarily involved. Two 
forms may be distinguished. The more frequent is that in which 
diffuse induration of the testicle occurs ; in the less frequent 
variety there are circumscribed gummata. In the diffuse form 
the organ is more or less uniformly indurated, and on section 
dense bands of fibrous tissue are conspicuous. The tubules suffer 
compression, degeneration, and atrophy, and sometimes become 



DISEASES OF THE REPRODUCTIVE ORGANS. 687 



converted into cheesy foci. The gummata have the usual translu- 
cent or cheesy appearance. When the membranes are involved 
diffuse thickening occurs ; and in rare cases the disease extends to 
the skin, causing superficial granulations {syphilitic fungus). The 
vas deferens is often greatly thickened, as are also the walls of 
the blood-vessels of the testis and epididymis. 

I^epra of the testis occasions nodular lesions and pressure- 
atrophy of the tubules. Lepra-cells containing bacilli, as well as 
free bacilli, occur in the tubules in abundance. This fact is im- 
portant as indicating a possible mode of transmission of the disease. 

TUMORS. 

Fibroma is occasionally observed in the rete testis and tunica 
albuginea as a small nodular tumor. 

Chondroma is rare. It may occur in the epididymis or rete, 
as a single node or as multiple small nodules. More frequently, 
small cartilaginous areas are found in carcinomata or other tumors 
of the testis. 

Osteoma is very rare. 

Myxoma is rare, except in association with other tumors. 

Rhabdomyoma sometimes occurs in the form of flesh-like 
growths of the testis. 

Sarcoma may occur in any of its various forms in the testis, 
and less commonly in the epididymis. It forms rapidly growing 
whitish or reddish tumors. Secondary changes, such as fatty de- 
generation, hemorrhage, cystic softening, and caseation, are not in- 
frequent. Cystic dilatation of the seminal tubules may occasion 
marked changes in the appearance of the tumor. The cysts are 
small, and filled with turbid liquid containing fat, desquamated 
cells, and cholesterin ; or large, and contain serous liquid, either 
clear, turbid, or blood-tinged. The lining epithelium of the cysts 
is columnar, or, in case of cysts of the epididymis, often ciliated. 
The walls of the tubules in some instances undergo active hyper- 
plasia, giving rise to papillomatous elevations of the inner surface, 
and a truly adenomatous proliferation may occur. In the latter 
cases the tumor may be designated adenosarcoma. Growths of this 
variety are sometimes met with in young adults or children, and 
most frequently in the rete testis. They are more or less malig- 
nant, causing frequent metastasis through the lymphatics or blood- 
vessels. 

Adenoma of the testicle is rare ; much more frequently cystic 
tumors have a more or less adenomatous character (see Cysts). 

Carcinoma may occur in the form of a scirrhus, but more fre- 
quently as a soft or medullary variety (Fig. 330). Mucoid and col- 
loid degenerations are rather frequent, and cystic softening may 
occur. Cysts may also result from dilatation of the tubules. Carti- 



688 TEXT-BOOK OF PATHOLOGY. 

laginous areas are sometimes found in the stroma of the growth ; to 
such the term chondrocarcinoma is applied. More or less com- 
plete destruction of the testicle and epididymis is frequent, but the 
tunica albuginea usually resists invasion for a considerable time. 
Carcinoma of the testicle seems to originate from the epithelium 




Fig. 330.— Carcinoma of the testicle (from a specimen in the Museum of the Philadelphia 

Hospital). 

of the convoluted tubules. Metastasis through the lymphatics 
and blood-vessels is frequent, and extension through the testicular 
envelopes to the skin may occur. 

Cysts. — Retention-cysts of the tubules are frequent in cases 
of inflammation and induration of the testis and epididymis. Some- 
times they contain a simple milky liquid ; in other cases sperma- 
tozoa are found in the fluid, and to these cysts the term sperma- 
tocele is applied. The cysts may be numerous and small, or may 
be very large, containing a hundred or more cubic centimeters of 
liquid. The cysts are found in the body of the organ ; but, when 
large, project from the surface. Very large cysts push the testicle 
and epididymis to one side. Occasionally cysts originate from the 
hydatids or the paradidymis. These may be spermatoceles, when 
one of the vasa aberrantia opens into them. 

Secondary proliferations of the epithelium of the cysts may 
convert a simple into a papuliferous cystoma; and occasionally 



DISEASES OF THE REPRODUCTIVE ORGANS. 689 



the primary process seems to be one of adenomatous character, the 
cystic condition being the result of secondary distention or of the 
peculiar character of the acini formed. 

Small cystic cavities may contain mucous liquid or thick, curdy 
material. In the latter case the term atheromatous cyst is appli- 
cable. 

Dermoid cysts are occasional tumors of the testis proper. 
They may be simple sacs, lined with epidermal tissue and filled 
with pultaceous matter ; or complicated dermoids, containing 
teeth, bone, muscle-fibers, and nerve-tissue. 

PARASITES. 
EchinococcilS-cysts are rarely met with. 



THE PROSTATE GLAND. 
INFLAMMATION. 

Inflammation of the prostate, or prostatitis, is most 
frequently secondary to posterior urethritis. Sometimes, however, 
it results from other causes, such as metastatic involvement in 
general pyemia or other forms of infection. Inflammations in the 
vicinity and direct injuries of the prostate may likewise cause 
acute inflammation. 

Pathologic Anatomy. — A simple and a suppurative form may 
be distinguished. 

Simple Prostatitis. — In the ordinary prostatitis following 
urethritis the disease takes the simple form, the gland being con- 
gested and swollen, and causing by its enlargement more or less 
obstruction of the urethra. Small suppurative foci may be formed 
in and about the glandular pouches and tubules. 

Suppurative or phlegmonous prostatitis, or abscess of the 
prostate, may be a terminal condition of the previous form, or it 
may be developed primarily. In cases of metastatic prostatitis 
a number of foci of suppuration may occur and subsequently coa- 
lesce, or a diffuse suppurative infiltration may take place. The 
development of abscesses is usually acute, though in some cases it 
may occur insidiously. If the abscesses are small they may sub- 
sequently undergo encapsulation, inspissation, and even calcifica- 
tion. Larger abscesses are prone to rupture into the urethra, 
usually through a number of openings. Sometimes, however, the 
inflammation extends to the tissues around the gland, causing 
periprostatitis, and later rupture into the rectum may occur. Ex- 
tensive phlegmonous inflammation of the pelvic tissues is an 
unusual result. 

44 



690 



TEXT-BOOK OF PATHOLOGY. 



ATROPHY AND DEGENERATION. 

Atrophy of the gland is occasionally met with in youthful 
individuals, and may be the result of disease or removal of the 
testis. It also occurs in the aged, and in this case atrophy of the 
tissues surrounding the prostatic ducts may be accompanied by dila- 
tation of the ducts themselves. The gland then presents a cavern- 
ous appearance. Atrophy of the gland sometimes leads to incon- 
tinence of urine. 

Fatty degeneration of the epithelium of the gland and of 
the muscle-fibers is frequent in old age, and may occur as an in- 
dependent condition or in association with hypertrophic enlarge- 
ment of the gland. The gland becomes soft, and diffusely yellow 
or mottled in color. 

CONCRETIONS. 

Prostatic concretions are not unusual in persons of advanced 
age, and are frequently found in considerable numbers. They 
vary in size from almost microscopic granules to bodies the size 
of a millet-seed. On section through the gland these brownish- 
colored bodies give the appearance of a surface sprinkled with 
snuff. The granules are usually round or oval, and are character- 
ized by concentric lamellations. They may be colorless at first, 
but usually become brownish. The term amylaceous bodies has 
been applied to them, and they have been supposed, though 
erroneously, to be composed of amyloid material, such as occurs in 
amyloid degeneration. When they reach considerable size calca- 
reous salts may deposit around them and give them an irregular 
form. Sometimes the concretions are discharged through the 
prostatic ducts into the urethra ; in other cases the larger concre- 
tions project prominently into the urethra beneath its mucous mem- 
brane. 

INFECTIOUS DISEASES. 

Tuberculosis of the prostate is usually found in association 
with tuberculosis of the other genital organs, es]3ecially the vas 
deferens and epididymis. It is also met with in association with 
tuberculosis of the bladder or kidney. The prostate is usually 
diffusely enlarged, and may be somewhat nodular upon the surface. 
On section caseous areas are found, or the entire gland has a 
caseous appearance. Recent tubercles are rarely visible, as casea- 
tion progresses with unusual rapidity in this organ. Primary 
tuberculosis of the prostate is rare. 

HYPERTROPHY AND TUMORS. 

Hypertrophy of the prostate is a condition sometimes inflam- 
matory in character, sometimes more probably of the nature of 



DISEASES OF THE REPRODUCTIVE ORGANS. 691 

tumor-formation. It occurs most frequently in the aged. The 
causes are often quite obscure. In some cases chronic posterior 
urethritis seems to be the important factor ; in other instances 
disturbances of the circulation, and especially varicose conditions 
of the veins, are active in the causation. 




Fig. 331.— Hypertrophy of the middle lohe of the prostate: A, middle lobe of prostate; 
B, urethra (White and Wood). 

The organ may enlarge in a uniform manner, or there may be 
nodular or localized swelling. Of the localized form the most im- 
portant, from a clinical aspect, is that in which the middle lobe or 
the isthmus of the gland enlarges and projects under the posterior 
wall of the urethra as a small or large rounded elevation, or as a 



692 



TEXT-BOOK OF PATHOLOGY. 



transverse bar or obstruction (Fig. 331). According to the inves- 
tigations of some authorities, the enlargement in such instances is 
due to a hyperplasia of accessor)' prostatic tissue lying immediately 
under the mucous membrane of the bladder and of the prostatic por- 
tion of the urethra, with subsequent involvement of the isthmus of 
the gland itself. 

On section through the gland there may be a uniform indura- 
tion, or in other cases, in consequence of associated changes in the 
epithelial or glandular elements, there may be scattered through 
the gland areas of softening or of proliferation of the glandular ele- 
ments, or cystic distentions of the gland-tubules. In such instances 
the indurated gland presents more or less softened or cystic foci. 

Microscopically, in the diffuse form, involving the stroma alone, 
the gland presents merely the features of uniform hbromyomatous 




Fig. 332.— Section of hypertrophied prostate of a man aged 74 years ; natural size : a, 
urethra; b, colliculus seminalis (Socin). 

proliferation, and corresponds in structure with fibromatous or myo- 
fibromatous tumors of the uterus (Fig. 332). In other cases the 
glandular elements take an active part in the pathologic process, and 
a distinctly adenomatous character is added. The glandular ele- 
ments may undergo fatty degeneration, and the lumina of the acini 
and tubules may be filled with milk-like, fatty material. In other 
cases pronounced cystic distention of the gland occurs. 

Results of Hypertrophy of the Prostate. — Enlargements of the 
prostate usually interfere with the discharge of urine. This is 
particularly marked in cases in which the middle lobe projects 
into the urethra, though in some instances the opposite result may 
be produced, viz., incontinence of urine due to interference with 



DISEASES OF THE REPRODUCTIVE ORGANS. 693 



the contractions of the sphincter of the neck of the bladder. In 
cases of enlargement of one of the lateral lobes obstruction to the 
flow of urine is caused by lateral deviation and compression of the 
urethra. 

The muscular walls of the bladder at first become hyper- 
trophied and dilatation of the bladder subsequently occurs. 
Cystitis, distention of the ureters and renal pelves, and ascend- 
ing infection, causing ureteritis, pyelitis, and pyelonephritis, are 
among the late results. 

Sarcoma. — Sarcoma is a rare tumor of the prostate. It 
generally has the characters of lymphosarcoma, and is a rapidly 
growing, destructive tumor. In a few cases combination with 
adenoma has been observed. 

Carcinoma of the prostate is more frequent than sarcoma, 
though it is not a common tumor. It occurs in relatively young 
persons. The tumor arises from the epithelium of the tubules, 
and takes the form of nodular, grayish or white masses which 
cause irregular enlargements of the gland, and not rarely project 
into the urethra or the base of the bladder. Superficial ulcera- 
tion of the mucous membrane over these projections is not infre- 
quent. The stroma of the gland usually proliferates actively. 
Metastasis to the inguinal glands, or to distant parts, including 
the bones, is not infrequent; but direct extension to the bladder, 
seminal vesicles, or rectum is more common. 

Cysts of the prostate are usually the result of retention of exu- 
dates within the glands or their ducts. Occasionally cystic forma- 
tions seem to arise from remnants of Miiller's ducts. 

COWPER'S GLANDS. 

Inflammatory conditions are met with in these glands in asso- 
ciation with similar affections of the prostate. Occasionally, inde- 
pendent inflammation of Cowper's glands results from posterior 
urethritis. The gland is enlarged and presents the usual appear- 
ances of inflammation. The termination may be abscess-formation. 
Obliteration of the mouths of the ducts may occasion cystic con- 
ditions in the glands, and carcinoma has been described. 

THE SEMINAL VESICLES. 

Inflammation. — Acute inflammation of the seminal vesicles 
may occur in association with gonorrheal urethritis. The vesi- 
cles become distended with seminal secretion and mucopurulent 
exudate. Their walls are swollen, and the mucous membrane 
presents the appearance of catarrhal inflammation. 

Chronic inflammation may result from the acute form, and 
causes contraction and thickening of the walls. 



694 



TEXT-BOOK OF PATHOLOGY. 



Tuberculosis of the seminal vesicles is common in cases of 
urogenital tuberculosis. The vesicles are rarely independently 
affected. The walls become thickened and may present nodular, 
cheesy masses, and there may be ulcerations of the mucous surface. 
The cavities of the vesicles contain caseous or puriform material. 

Tumors. — Primary carcinoma has been described ; but second- 
ary carcinoma, resulting from extension of cancer of the adjacent 
structures, is more common. 

Cystic distention and the formation of diverticula result from 
obstructions of the ejaculatory duct. The contents of the vesicles 
in such cases are seromucous in character. 

Concretions frequently result from calcification of inflamma- 
tory exudates. They are especially frequent in association with 
tuberculosis. 

THE MAMMARY GLANDS. 
CONGENITAL ABNORMALITIES. 

Absence of one or both breasts may occur in association with 
other defects of development of the thoracic walls. Incomplete 
development of the mammary glands, or hypoplasia, may be asso- 
ciated with hypoplasia of the genital organs. 

Supernumerary mammary glands are frequently observed ; 
the term polymastia is given this condition. The supernumerary 
gland or glands may be situated between the normal glands, below 
these, or in distant parts, such as the back, shoulders, and arms. 
They may occur in either sex, and may be structurally complete 
and functionally active ; or may be merely rounded masses of 
mammary tissue without excretory ducts or nipples. In the latter 
instances the probable explanation of the condition is that in the 
process of development parts of the normal glands have been split 
off and have separately developed. 

Early Development. — The mammary glands may be de- 
veloped at an abnormally early period, in correspondence with 
early development of the genital organs. 

Abnormal functional activity (secretion) may be stimu- 
lated by various diseases of the genital organs ; and in the new- 
born of either sex during the first week of life slight secretion of 
colostrum-like material is frequent. 

Abnormal development of the male breast is occasion- 
ally observed, especially about the age of puberty, and sometimes 
copious secretion of milk takes place. Usually the organ subse- 
quently atrophies, but exceptionally the enlargement and secretion 
persist. 

CIRCULATORY DISTURBANCES. 

Hyperemia occurs during the menstrual period and at the 
beginning of lactation, as a physiologic process, and causes slight 



DISEASES OF THE REPRODUCTIVE ORGANS. 695 



swelling and redness. Pathologic hyperemia plays a part in the 
process of inflammation. 

Hemorrhages are usually the result of traumatism. They 
may occur into the gland itself, or into the connective tissue in 
front of or behind the gland. Occasionally hemorrhages are due 
to intense inflammation or to tumor-formation. The blood may 
find its way into the lactiferous tubules, and may be in part dis- 
charged from the nipple. In case of large hemorrhages the blood 
may subsequently undergo absorption or inspissation, and hemor- 
rhagic cysts may be formed. 

INFLAMMATIONS. 

Acute inflammation of the mammae, or acute mastitis, 

is rarely met with, excepting during the puerperium. Exception- 
ally it may occur in cases of general pyemia, or in the new-born 
as a result of active secretion and obstruction to the outlets. 
Sometimes inflammation of the glands results from direct exten- 
sion of inflammatory processes of the skin, subcutaneous tissue, or 
thoracic walls. Puerperal mastitis is infective in character, and 
results from injury or disease of the nipple, from which the infec- 
tive agents enter the glands. The actual portal of entrance may 
be the discharging tubules, or may be fissures and erosions of the 
nipple. Various micro-organisms have been discovered, including 
staphylococci and streptococci. 

Pathologic Anatomy. — The gland is swollen and distends its 
capsule tensely, the skin is reddened, and a general hyperemia of 
the gland is noted. During the earlier stages the inflammation 
may be localized or may be diffuse. In the former case more or 
less circumscribed induration is discovered, while in the latter the 
organ is uniformly indurated. The tendency of mastitis is to a 
termination in suppuration. On section through the gland areas 
of light-yellow T ish color indicate the purulent infiltration, while in 
the later stages more or less extensive abscesses are formed. The 
latter may communicate with the lactiferous tubules, and pus and 
milk may be discharged from the nipple. The abscesses tend to 
extend in various directions, and may finally rupture upon the sur- 
face through fistulae. After discharge of the pus granulation- 
tissue is formed, and the cavities are obliterated by cicatricial 
tissue. When the larger discharging tubules are opened by the 
abscesses fistulse may be formed, which continuously discharge 
milk. Small collections of pus may become encapsulated and 
inspissated, being converted into cheesy or partly calcified matter. 

The connective tissues around the mammary gland are some- 
times involved by extension, and suppurative or necrotic perimas- 
titis results. Extension to the thoracic walls and pleura is rare. 

Chronic Mastitis. — Diffuse induration of the mammary 



696 



TEXT-BOOK OF PATHOLOGY. 



gland, resembling in its histologic features the indurative or 
chronic interstitial inflammations of other organs, is occasionally 
seen in middle-aged or old women. The causes are obscure, and 
it is difficult to distinguish some of the cases from certain forms 
of fibromatous tumors. The gland becomes hardened and some- 
times slightly increased in size. In other cases retraction of the 
connective tissue causes a reduction in the size. On section firm 
bands of connective tissue are conspicuous, and the lactiferous 
tubules may be distended, forming small or large retention-cysts. 
This form of disease will be further discussed under Fibroma. 

ATROPHY AND HYPERTROPHY. 

Atrophy of the gland occurs as a physiologic process after the 
menopause, or it may result from local causes, such as abscess or 
tumor-formation. Artificial menopause, following oophorectomy 
or diseases of the reproductive organs, may occasion atrophy simi- 
lar to that normally present in old age. The gland may simply 
decrease in size, without notable change of any other kind. Some- 
times, however, connective-tissue hyperplasia accompanies the 
atrophy of the glandular elements, and diffuse infiltration may 
occur. 

Hypertrophy of the gland is sometimes met with in girls at 
the age of puberty, and leads to a uniform enlargement of the or- 
gan. In some cases there is a true hypertrophy of all the con- 
stituents of the gland ; in other instances dilatation of the lym- 
phatic channels, or degenerative changes, may cause a simulation 
of true hypertrophy. Both breasts, as a rule, are affected, and 
there may be increased functional activity [galactorrhea). 

DEGENERATIONS. 

Fatty infiltration, or lipomatosis, of the gland may accom- 
pany atrophy, or may occur as an independent condition. The 
gland may be greatly enlarged. Accompanying this degeneration 
there is usually diffuse hyperplasia of the connective tissue. 

Myxomatous degeneration may be associated with fatty 
infiltration. 

INFECTIOUS DISEASES. 

Tuberculosis of the mammary gland may be associated Avith 
tuberculosis of the axillary glands, or of other parts, or may be 
primary. The tubercle-bacilli reach the gland either through the 
lactiferous tubules or through the blood. The disease is charac- 
terized by the formation of distinct tubercles, which tend to unite 
and form caseous areas. There is rarely extensive disease. 

Syphilis, in the form of gummata, is sometimes met with in 
acquired or congenital syphilis. 



DISEASES OE THE REPRODUCTIVE ORGANS. 697 



TUMORS. 

Fibroma may be met with in the form of circumscribed nodu- 
lar growths, or, according to the view of some pathologists, as a 
diffuse process. Circumscribed fibroma presents itself as a hard, 
nodular tumor, often having a distinct capsule, and on section 
presenting a lamellar arrangement. The glandular elements of 
the organ in the area of invasion may undergo secondary hyper- 
plasia, and thus a form of fibro-adenoma may be developed. In 
the cases termed diffuse fibroma the entire organ may be indurated, 
or nodular areas of sclerosis may be found in various parts of the 
gland. The acini and ducts may at the same time undergo pro- 
liferation, forming adenomatous structures ; or compression of the 
ducts may lead to retention-cysts. It is difficult to determine in 
individual cases whether the process is one of tumor-formation or 
one of inflammatory hyperplasia. 

A form of particular interest is that known as intracanalicil- 
lar fibroma. In this the proliferating fibrous tissue projects into 
the normal or dilated tubules in the form of papillary elevations. 
The mucosa lining the tubules is pushed forward by the ingrowths, 
and covers these in the same manner as epithelium covers super- 
ficial papillomata of the skin or mucous membranes. The gland 




Fig. 333.— Intracanalicular fibroma of the mammary gland (Kaufmann). 



may be greatly enlarged, and on section presents an appearance 
resembling that of a cut through a cauliflower (Fig. 333). 

I<ipoma of the mammary glands occurs in the form of round, 



698 



TEXT-BOOK OF PATHOLOGY. 



encapsulated tumors of the interstitial or periglandular connective 
tissues. 

Myxoma may occur in a diffuse form, causing a transforma- 
tion of the gland into myxomatous material, or as circumscribed 
tumors. 

Myomata containing smooth muscle-fibers, and mixed tumors 
containing striated muscle-fibers, are rare. 

Chondroma and osteoma have been observed. 

Sarcoma is most frequently of the round-cell variety. It 
occurs in a diffuse form or as circumscribed nodules ; association 
with fibroma and myxoma is not infrequent. 

In diffuse sarcoma the gland undergoes a uniform enlargement, 
and the neoplasm extends rapidly, forming attachments to the 
skin and sometimes causing superficial ulceration. In other cases 
extension toward the chest-walls may occur, and may finally reach 
the pleura. On section through the gland a lobular character of 
the tumor may be recognized, and areas of fibrous or myxomatous 
character are visible here and there. Cystic conditions, sometimes 
met with, may be due to obstruction and consequent distention of 
the lactiferous tubules. The term cystosarcoma is appropriately 
applied to such cases. The sarcomatous tissue may project into 
the dilated tubules in a polypoid form (intracanalicular sarcoma). 
Section through the gland in such cases presents an appearance 
not unlike the surface of section of a head of cabbage. Cysts may 
also be formed in sarcomata by degenerative softening. 

Localized sarcomata occur as nodular tumors arising from the 
connective tissue surrounding the acini. On section through the 
tumor the glandular acini may be seen within the nodules. 

In any form of sarcoma the epithelium of the tubules and acini 
may undergo secondary proliferation, when the term adenosarcoma 
is applicable. 

Adenoma of the mammary glands may be an independent 
growth, or may be associated with fibroma, sarcoma, or other tu- 
mors. The independent form presents itself as a circumscribed, 
encapsulated, nodular tumor, somewhat firmer than the substance 
of the normal gland. Microscopically it consists of more or less 
typical glandular acini. These are usually somewhat dilated, and 
the epithelial cells are larger than those of the normal gland (Fig. 
64). Instead of a single layer of columnar cells, active hyperplasia 
may cause a complete filling of the acinus with epithelial cells. 
Fatty degeneration of the cells is not infrequent, and sometimes 
there is a certain amount of milk-secretion, causing additional dis- 
tention of the cavities. 

Carcinoma. — Carcinoma may develop from the tubules or 
from the acini of the glands. It may begin as an adenomatous 
tumor, wmich subsequently undergoes carcinomatous transforma- 
tion, or may be a typical glandular cancer from the beginning. 



DISEASES OF THE REPRODUCTIVE ORGANS. 699 



In the cases primarily adenomatous the structure of the acini be- 
comes atypical and the epithelial cells tend to penetrate the mera- 
brana propria and form irregular collections or columns in the 
interstitial tissue. Degenerative changes are often observed, 
among which fatty degeneration is most frequent. Mucoid de- 
generation and a form of caseation are sometimes met with, and 
calcification may take place in the interstitial tissues. Occasion- 
ally an attempt at formation of milk occurs in the cancer-acini. 

Varieties. — Among the varieties of carcinoma are the medul- 
lary, the simple, the scirrhous, and the myxomatous. 

Medullary carcinoma, or soft cancer, is characterized by its 
softness and the abundance of liquid (cancer-juice). It grows 
rapidly and soon invades a large part of the gland, and attaches 




Fig. 334.— Ulcerated carcinoma of the breast. 



itself to the skin, which may finally be broken, exposing an 
ulcerated surface (Fig. 334). Actual inflammatory changes ter- 
minating in suppuration are not infrequent. 

Scirrhous cancer is slower in growth, and is usually very 
hard ; the skin is firmly attached to the tumor, and the nipple is 
usually retracted. On section the tumor is found to be of a firm, 
fibrous, and somewhat translucent character ; extensions of the 
growth are seen radiating in various directions from the body of 
the tumor. Microscopically the growth consists of fasciculated 
connective tissue, enclosing round or elongated collections of 
cancer-cells (Fig. 72). 



700 



TEXT-BOOK OF PATHOLOGY. 



Simple carcinoma stands between the medullary and the 
scirrhous forms in point of hardness, as well as in point of malig- 
nancy. The three forms differ only in the relative amount of 
epithelial elements and fibrous tissue. 

Myxomatous, colloid, or gelatinous cancer is a rare form in 
which the interstitial connective tissue suffers mucoid change, and 
the epithelial cells of the cancer-acini undergo more or less fatty 
or exceptionally mucoid degeneration (Fig. 73). 

Results. — Cancer of the breast may extend directly to the sub- 
cutaneous tissues and skin on the one hand, or to the walls of the 
chest and pleura on the other hand. Metastasis frequently takes 
place through the lymphatics, the axillary glands, as a rule, 
presenting the first evidence of metastasis. Malignancy varies 
with the softness or hardness of the tumors, the scirrhous form 
frequently having a comparatively benign character. Sometimes 
the increasing growth of connective tissue in this variety leads to 
practical cessation of the growth of the tumor. 

Mammary cancers are much more frequent in the female than 
in the male sex. They are commonly met with after the age of 
forty, and traumatic influences seem to bear some relation to their 
occurrence. 

Cysts. — Repeated reference has been made to the retention- 
cysts of the lactiferous tubules caused by compression or other 
forms of obstruction. The gland may contain a few or many 
cystic cavities about the size of a pea, containing whitish or 
milky liquid. Occasionally the contents of the cysts are cheesy 
{atheromatous). Distention of the acini of the glands in conse- 
quence of obstructions to the outflow of milk may lead to large 
cystic tumors containing milk (galactocele). In the later stages 
the contents of such cysts may become thickened or caseous. 



CHAPTER IX. 

DISEASES OF THE BONES. 

Anatomy and Development. — Bone is a dense form of 
connective tissue, the cement-substance being impregnated with 
lime-salts. It may be spongy or compact in character. On 
transverse section one sees certain oval openings, surrounded by 
concentric lamellae of a substance containing lime-salts. Each 
opening is the end of a so-called Haversian canal, which with the 
surrounding lamellae forms a Haversian system. The areas be- 
tween the Haversian systems are filled with osseous tissue not 
arranged concentrically. Between the lamellae of bony tissue are 



DISEASES OF THE BONES. 



701 



seen irregularly oval spaces — lacunae — from which run branching 
canaliculi. In preparations of fresh bone the lacunae are found to 
be occupied by the bone-cells, which are irregular and have branch- 
ing projections extending some distance into the canaliculi. In 
the center of the bones are found hollow spaces containing the 
bone-marrow. This is a vascular tissue, in the meshes of which 
are found large and small rounded cells resembling the lymphoid 
cells, red corpuscles, ordinary leukocytes, and some nucleated red 
corpuscles. A form of cell of particular interest is the large mul- 
tinucleated giant-cell, or myeloplaque. The marrow extends in 
the form of projections into the substance of the bone and com- 
municates with the Haversian canals. 

Surrounding the bone is the fibrous periosteum. This consists 
of a dense outer layer and a more cellular inner one, which is osteo- 
genetic in function. 

Development. — The beginning of the change of the original car- 
tilage into bone consists in the multiplication of the cartilage-cells 
and their arrangement in longitudinal rows. They grow into car- 
tilage-corpuscles of considerable size, calcification at the same time 
occurring in the matrix between these cells. Simultaneously vas- 
cular projections extend inward from the perichondrium ; the car- 
tilage-cells and preliminary calcareous deposit are subsequently 
removed, primary marrow-spaces being thus formed. Bone-cells 
are deposited in the spaces between the original cartilaginous tra- 
becular, and at once begin to cover themselves with bony deposits, 
the cartilaginous trabecular gradually diminishing by absorption. 
By these processes a spongy form of bone is developed. Subse- 
quently the concentric calcareous lamellae of the Haversian sys- 
tems are deposited within the spaces, and the spongy bone is thus 
converted into the dense form. 

DISORDERS OF DEVELOPMENT. 

Many congenital defects of development are observed, such as 
the appearance of supernumerary bones, the absence of certain 
bones, the failure of union between epiphyses and diaphyses, etc. 
These conditions are of little pathologic interest. The most im- 
portant developmental disease is rickets. 

RICKETS. 

Definition. — Rickets or rachitis, is a constitutional disorder, 
attended with abnormal developmental processes in the bones, of 
which active proliferation of the cellular elements and lack of 
normal calcification are the most important. 

Etiology. — The causes of rickets are still very obscure. The 
disease is in some way connected with improper nourishment, though 



702 



TEXT-BOOK OF PATHOLOGY. 



there is probably also an inherited disposition. It has been sought 
to establish a connection between rickets and syphilis, but any such 
relation is doubtful. Various chemical theories have been offered 
in explanation. Formerly it was supposed that the presence in the 
digestive tract of lactic acid in excess prevented the proper absorp- 
tion of calcium ; this theory, however, is generally abandoned. 
The disease occurs in infants during the first year of life, and 
continues during the second and third years, after which the 
active manifestations subside. 

Pathologic Anatomy. — Rickets leads to various deformities, 
principally situated in the long bones and skull. The epiphy- 
ses, as those of the wrist, ankle, etc., are swollen, and in more 
advanced stages the shafts of the long bones may be variously 
distorted. , 

Sharp bends {infractions) may be observed in the long bones, 
and complete fractures may occur. The alteration of the skull is 
characteristic. The head is large and square in shape, the fore- 
head prominent, and the fontanelles remain open a long time. 
Osteophytes may form, and not rarely areas are found in the tem- 
poral or other bones in which the mineral substance is deficient 
or almost completely wanting (craniotabes), the spaces being filled 
by a parchment-like membrane. Deformities of the chest are 
frequent, the chicken-breasted condition being the most marked. 
In the beginning of the disease slight enlargement of the ends of 
the ribs at the junction with the costal cartilages, causing the 




Fig. 335.— Kachitic enlargement of the end, of a rib (modified from Bollinger). 

beaded appearance called the " rachitic rosary," is observed (Fig. 
335). Various distortions of the spinal column, flattening of the 
pelvis, and other deformities may be met with in marked cases. 

The minute changes of rickets consist in a form of abnormal 
development, in which calcareous deposition does not progress in 
the normal manner, but is replaced by proliferation of the cellular 
elements. In consequence of this the bone presents irregular areas 
of partial calcification lying between portions made up of greatly 
proliferated and enlarged cartilage-cells. Projections from the 
marrow and periosteum extend deeply and visibly into the body 
of the bone, which is thus composed for the most part of osteoid 
instead of osseous tissue. The marrow-spaces are irregular and 
excessive in size. These changes in the bone are marked at 



DISEASES OF THE BONES. 



703 



the epiphyseal extremities, and thus lead to the visible enlarge- 
ments. It is thus seen that the process in rickets is failure of 
development of the normal structure, rather than absorption of 
existing bone. The original calcareous deposit around the carti- 
lage-cells is largely or completely absorbed, as in normal bone-for- 
mation, and often even more rapidly. The subsequent deposit of 
calcareous bone does not form, but in place of it there occurs a 
rapid proliferation of cartilaginous and other cells. 

Associated Conditions. — The changes in the bones do not 
constitute the entire pathology of rickets. There are frequently 
gastro-intestinal disorders, such as catarrhal inflammations of the 
mucous membrane. Proliferative changes are met with in the 
spleen and liver, leading to fibrous overgrowth and enlargement, 
and the blood is more or less profoundly altered. Decrease in the 
number of red corpuscles and leukocytosis are the conspicuous 
features. Nucleated red corpuscles may be found in more or less 
abundance, according to the grade of anemia, and the leukocytosis 
involves a special increase of mononuclear elements, and myelo- 
cytes may be present. 

Congenital rickets differs in some respects from the dis- 
ease met with after birth. The extremities are short and thick, 
the ends of the bones enlarged, and the shafts bent. There is 
increase of the original cartilage and of the periosteum, with an 
arrest of development of the bones. 

REGENERATION OF BONE. 

Regeneration of bone occurs most typically in the healing of 
fractures, and also as a part of various pathologic processes in 
which a certain amount of destruction of bony tissue has taken 
place. Hypertrophy may be included in the same group of affec- 
tions. 

Fractures. — Definition. — Fractures are breaches in the con- 
tinuity of bone which occur in consequence of direct force or 
of muscular contractions. The bone may be broken in vari- 
ous directions, the line of fracture being straight or irregular, 
directly transverse to the long axis of the bone, or oblique. The 
bone may be broken into a number of splinters (comminuted fract- 
ure), or the fracture may be a single one. There is always more 
or less injury to the soft parts immediately surrounding the bone, 
and sometimes extensive injury causes communication between the 
outer surface and the seat of fracture through flesh wounds (com- 
pound fracture). 

Repair of Fractures. — The process of repair is much the same as 
the process in the original formation of bone. Immediately after 
the fracture there is more or less hemorrhagic extravasation with- 
in the marrow and around the broken ends of the bone. Within 



704 



TEXT-BOOK OF PATHOLOGY. 



a few days cellular infiltration, with congestion and edematous 
swelling of the periosteum and marrow, as well as of the bones, 
may be noted. Proliferative changes then take place in the same 
situations and new blood-vessels are formed. The tissue soon 
becomes somewhat hardened from deposit of calcareous matter and 
cartilaginous formation. Its condition varies greatly in different 
cases ; sometimes it is quite fibrous, in other cases almost purely 
cartilaginous. Gradually it is converted into bone by the regular 
processes of bone-formation. At this stage the seat of fracture is 
occupied by a deposit of soft, bony material of considerable bulk, 
which causes a local thickening of the bone. Finally the excess 




Fig. 336— Fracture of the femur, show- Fig. 337.— Fracture of humerus; see- 

ing malposition of the ends of the bone tion through the bone, showing the repair 

and abundant callus (modified from Bol- of the fracture (modified from Bollinger), 

linger). 

is removed by absorption, the parts in the direct line of the bone 
upon which the strain naturally falls becoming thickened, while 
other parts are absorbed. 

The original deposit of osteoid or chondroid material at the seat 
of fracture is termed callus (Fig. 336). Part of this is deposited on 
the exterior (periosteal callus), and is derived from the periosteum ; 
part is within the marrow-cavity (myelogenous callus) ; and a third 



DISEASES OF THE BONES. 



705 



part is sometimes seen between the ends of the bone (intermediary 
callus). The last is produced by the periosteum. 

The healing of fractures under the most favorable circum- 
stances — that is, in cases in which the fragments of bone are 
restored to their proper position — is accomplished with but little 
disturbance of the normal relations. The seat of fracture may 
be permanently thickened, and there is always some shortening of 
the affected bone. When the fragments are not placed in proper 
position, angular deformities, with considerable thickening from 
deposit of bony material between the fragments, result (Fig. 337). 

When the fragments are not kept in apposition, or when the 
general condition of the patient is unsatisfactory, the union of the 
fragments may be prevented and "ununited fractures" result. 
The ends of the fragments in these cases become rounded by ab- 
sorption of the sharp edges, forming false joints (pseudarthroses). 

Hypertrophy. 

Local or general hypertrophy of bone may be found. Local 
hypertrophies may occur in consequence of increased strain upon 
certain parts of a bone, either directly or through the muscles. 
In muscular individuals hypertrophy of this kind is frequently 
seen at points of attachment of the muscles. In cases of in- 
jury or incapacity of one of the limbs the other may show 
hypertrophy. 

Giant growth of certain bones, or of the entire skeleton, may 
be observed. Local hypertrophy of this kind, dating from child- 
hood, is especially common in the upper extremities, and is fre- 
quently unilateral. It may be observed as a bilateral condition in 
the fingers. Complete giant growth usually begins about the age 
of puberty. The individual, previously developed as others, begins 
to grow abnormally until an excessive size is reached. The bones 
are not only very large, but often markedly thickened and irregu- 
lar. 

Acromegaly is an allied condition in which giant growth of 
the hands and feet, forearms and legs, and parts of the face, 
notably the lower jaw and bridge of the nose, is observed. A 
certain amount of hyperplasia of the soft tissues in the affected 
region accompanies this change. The etiology of this affection is 
still unsettled. Hyperplastic conditions, tumors, and other diseases 
of the hypophysis cerebri have been met with in a considerable 
proportion of the cases. In some of the skeletons of giants 
investigated with regard to this point enlargement of the sella 
turcica has been found, and this evidences the occurrence of en- 
largement of the pituitary body in some, at least, of such persons. 
The exact relation between pituitary disease and bony hyper- 
trophies remains obscure. 

45 



706 



TEXT-BOOK OF PATHOLOGY. 



CIRCULATORY DISTURBANCES. 

Hyperemia is normal during the development of bone, or 
may accompany inflammatory disturbances of the neighboring 
parts. The marrow becomes more or less light- or dark-red in 
color, and the periosteal vessels may be injected. The entire bone 
may have a pink or reddish color. 

Thrombosis may occur in the blood-vessels of the marrow. 

Hemorrhage beneath the periosteum and in the marrow is 
comparatively common. It may result from traumatic causes or 
from scorbutic or purpuric conditions, as well as from inflamma- 
tory affections of the parts involved. Considerable subperiosteal 
hemorrhages are found in cases of infantile scurvy. The sepa- 
ration of the periosteum from the bone may lead to necrosis of the 
superficial layers of the bone. A similar accumulation of blood 
beneath the periosteum is that found over the bones of the skull 
in the new-born — the cephalhematoma. This results from the 
traumatism of labor. Large accumulations of blood of this nature 
may be absorbed or may undergo suppuration. 

Hemorrhage into the substance of bone may accompany other 
diseases affecting it, such as caries, tumors, and the like. 

INFLAMMATIONS. 
Periostitis, 

Definition. — Periostitis, or inflammation of the periosteum, 
may be of various forms, and may lead to different results. Some- 
times the evidences of inflammation are very apparent ; in other 
cases the disease appears in the form of a chronic productive pro- 
cess, leading to overgrowth. 

etiology. — Periostitis may be the result of traumatism, with 
or without the establishment of a communicating wound. In the 
latter case the injury provides an area of lessened resistance, which 
may subsequently become infected. In the former case the infec- 
tion is direct, coming from the outside. Hematogenous infection 
without local injury is frequently observed. Infective periostitis 
may result from extension of an inflammation situated near the 
bones or from osteomyelitis. In all forms of bone-disease more 
or less local periostitis occurs as a complication. In some cases 
the etiology is obscure, as in the periostitis which occurs during 
pregnancy and leads to the formation of osteophytes. 

Pathologic Anatomy. — We may distinguish simple, sup- 
purative, and ossifying periostitis. 

Simple Periostitis. — The membrane becomes swollen, red, 
and sometimes infiltrated with blood. Microscopically there are 
round-cell infiltration and proliferation of the periosteal tissue. 
If the process has been extensive, and the irritation long con- 



DISEASES OF THE BONES. 



707 



tinned, a termination in fibroid thickening may be observed. This 
is not unusual in cases of fractures. 

Purulent Periostitis. — The disease may be circumscribed or 
diffuse. There are marked swelling and cellular infiltration, 
particularly in the deeper layers, and abscess-formation results. 
Separation of the periosteum from the bone ensues, and may 
lead to local interruption of the circulation between the peri- 
osteum and the bone, and consequent superficial necrosis of the 
bone with exfoliation results. In the diffuse form of periostitis 
widespread areas of the periosteum may be quickly involved and 
rapid destruction takes place. In these cases a considerable 
inflammation of the surrounding tissues is customary. In all 
instances there is a tendency to burrowing of pus toward the sur- 
face, and its eventual discharge. The retention of necrotic portions 
of the bone may lead to continued suppuration, but with removal 
of the dead portions healing usually occurs. Ostitis and osteo- 
myelitis are very frequent results of periostitis ; on the other hand, 
they may be in certain cases the original cause. 

Ossifying' periostitis leads to the formation of bony excres- 
cences, exostoses, or osteophytes. There is first a proliferation 
of the osteogenetic layer of the periosteum, then partial ossification, 
and finally complete bone-formation with firm attachment to the 
underlying bone. These changes may be circumscribed or diffuse, 
and cause irregular elevations or general thickening of the bone. 
Occasionally the surrounding connective tissues are implicated 
(par ostitis). Ossifying periostitis may occur in the vicinity of 
joints affected with chronic arthritis. It may occur as a result 
of diseases of bones attended with considerable destruction, such 
as tumors, tuberculosis, etc. Occasionally the causes are entirely 
obscure. An interesting form is that which occurs in the bones 
of the hands and feet, forearms, and legs in tuberculosis of the 
lungs and empyema, or more rarely in other diseases ; to this the 
term hypertrophic osteo-arthropathy has been applied. This is a 
form of osteoperiostitis of ossifying type, and it seems to be due 
to the action of circulating toxins developed in the diseases with 
which it is associated. 

Associated Conditions and Results. — The conditions met 
with in the adjacent bones and other parts have been referred to. 
General infection and intoxication may follow upon the suppurative 
cases, and death may then occur from septicopyemia. Permanent 
thickening of the bone may result in any case, or resolution may 
be practically complete. 

Osteomyelitis and Ostitis. 

Definition. — Acute osteomyelitis and ostitis are usually com- 
bined, and occur as an inflammatory condition affecting the mar- 



708 



TEXT-BOOK OF PATHOLOGY. 



row and its extensions into the communicating canals of the 
bone. The lamellar substance of the bone is only secondarily 
involved. 

Etiology. — Osteomyelitis is an infective disease resulting 
from hematogenous infection in the course of various diseases, 
from local infections in cases of trauma- 
tism (fracture, amputation), or from peri- 
ostitis. Various micro-organisms, includ- 
ing staphylococci, streptococci, typhoid 
bacilli, and the Bacillus coli communis, 
have been discovered. 

Pathologic Anatomy. — The mar- 
row first becomes red and edematous, 
then cellular infiltration and proliferation 
are superadded, and finally collections of 
pus or diffuse purulent transformation fol- 
low. The surrounding bone is involved, 
becoming more or less infiltrated, soften- 
ing, and not rarely undergoing necrosis 
(Fig. 338). Small or large sequestra may 
be formed, or the bone may necrose com- 
pletely. Periostitis is generally associated, 
and the tissues around the bone are usu- 
ally infiltrated and suffer suppurative or 
necrotic changes. Hypertrophic changes 
may occur in the periosteum and super- 
ficial layers of bone, causing a bony en- 
casement of central sequestra. In such 
instances a suppurating sinus, extending 
from the bone to the surface, usually 
remains. 

Associated Conditions. — Implica- 
tion of the neighboring parts is habitual — 
deep-seated abscesses, arthritis, etc. Gen- 
eral infection is usually the final result, 
and commonly leads to a fatal end. 
Marked changes in the blood have been observed — leukocytosis, 
large proportions of large mononuclear cells, myelocytes. 




Fig. 338.— Necrosis of femur, 
the result ot acute osteomye- 
litis (Warren). 



Chronic Ostitis. 

Chronic inflammatory processes are more apt to involve the 
bone than the marrow, though the beginning of the disease may 
be frequently in the latter situation. It may be suppurative, de- 
generative, or hypertrophic in character. 

Etiology. — Chronic ostitis may follow osteomyelitis and ne- 
crosis, necrotic sequestra keeping up a constant irritation. In 



DISEASES OF THE BONES. 



709 



these cases the disease is primarily infective. The chronic inflam- 
mations of bone due to tuberculosis and syphilis have special char- 
acters, which will be described below. In many cases the cause 
of chronic ostitis is obscure, though probably circulating toxic 
substances are the specific factors. Direct traumatism, periostitis, 
or other inflammatory diseases surrounding the bone may be the 
immediate causes. 

Pathologic Anatomy. — In the necrotic and suppurative 
form, following osteomyelitis, there is more or less softening of 
the bony substance by absorption of the calcareous matter, and at 
the same time proliferation, in the form of granulation-tissue, of 
the cellular elements of the marrow and its prolongations within 
the Haversian channels. Localized abscesses may be formed, or 
infiltration of pus in various directions with increasing necrosis of 
the intervening bone may occur. 

The degenerative form of ostitis is a variety in which the cal- 
careous matter is absorbed and the bone thus rendered more soft 
and porous. The term inflammatory osteoporosis is applied to this. 
In the process of absorption there are formed upon the outer and 
inner surfaces of the bone, or within its substance, areas of erosion, 
hollow spaces or indentations, showing bone-corpuscles and giant- 
cells lying upon the eroded bony tissue. These depressions are 
the so-called Howship's lacunae. The giant-cells, which are active 
in the absorptive process, have been termed osteoclasts, and are 
identical with the osteoblasts or osteoplaxes of developing bone. 
Simultaneously with this absorption of the lamellae of bone there 
is proliferation of the marrow-substance in the eroded areas, and 
at the same time there may be increased vascularization of this in- 
tervening tissue. Perforations are frequently established through 
the lamellae by the penetration of new-formed blood-vessels, so that 
neighboring excavated areas communicate. This form of inflam- 
mation of the bone is frequent in the neighborhood of necrotic 
areas or osteomyelitic collections of pus, and plays a part in the 
pathologic processes of osteomalacia and other bone-diseases. It 
is rarely an independent condition. 

The hypertrophic form of chronic inflammation leads to in- 
creased density of the bone, to which the term condensing ostitis, 
or osteosclerosis, is applicable. It may occur as a reactive process 
surrounding areas of osteoporosis or other local diseases of the 
bone, or in association with ossifying periostitis. Occasionally it 
occurs in certain bones or parts of bones without local or well- 
ascertained general causes. Such cases are met with in syphilitic 
persons. The anatomical changes consist in the deposition of in- 
creased quantities of bony tissue by the same processes as are 
operative in normal bone-formation. 

The disease designated as leontiasis ossium is a form of osteo- 
sclerosis affecting the bones of the head and face, and causing 



710 



TEXT-BOOK OF PATHOLOGY. 



irregular thickening and enlargement of these bones. The cause 
of this condition is obscure. 

HYPOPLASIA AND ATROPHY. 

Hypoplasia, or the lack of development of bones, may occur 
as a local or general condition. Local hypoplasia may be due to 
injuries or diseases which render a part of the body useless. Gen- 
eral hypoplasia is found in cretins and dwarfs. 

True atrophy of the bones may involve an entire bone or 
only portions of it. General atrophy of the whole or of parts of a 
bone occurs as a result of inactivity or want of use, as in cases of 
palsy, chronic rheumatism, and the like. The implication of cer- 
tain parts of the nervous system (trophic centers) is particularly im- 
portant, as the atrophy resulting in such cases is much more 
extensive than that occurring in cases of similar inactivity from 
other causes. 

Partial atrophy of the bone may be due to pressure by 
aneurysms, tumors, and the like. In these cases there is gradual 
absorption of bony substance, and the process is really one of in- 
flammatory osteoporosis. 

General Atrophy. — Absorption of the bony substance, with 
resulting osteoporosis, may occur in marasmic individuals, par- 
ticularly in seniles. In these cases it is held by most author- 
ities that the pathologic condition is dependent upon the fail- 
ure of replacement of bone to make up for the normal absorp- 
tion constantly taking place. In these cases the bone becomes 
extremely fragile from the increase of its marrow-spaces and its 
general porosity. This condition of fragility is termed fragilitas 
ossium, or osteopsathyrosis. Occasionally this condition of fragility 
is met with as an idiopathic disease, without definitely discover- 
able causation and without evident disease of the bones. Such 
cases have been found to occur in certain families through several 
generations. 

DEGENERATIVE CONDITIONS. 
Caries. 

Caries is a term applied to the molecular destruction of bone, 
corresponding to ulceration of the soft parts. It may be asso- 
ciated with osteomyelitis, or with necrosis due to traumatism or 
various infective conditions. The changes consist in progressive 
softening and crumbling of the bone, with eventual destruction of 
more or less considerable areas. Caries is especially frequent as 
a part of tuberculosis of the bones, and will be described in con- 
nection with that disease. 



DISEASES OF THE BONES. 



711 



Necrosis. 

Definition. — Necrosis is a term applied to the death of a 
small or large portion of bone in mass. 

Ktiology. — Among the causes are the various acute or chronic 
diseases of the periosteum, bone-marrow, and adjacent bone. In 
cases of purulent periostitis the separation of the periosteum from 
the underlying bone leads to interruption of blood-supply and 
superficial necrosis. Similar results occur in cases of osteomye- 
litis. Necrosis of the bone may also occur in consequence of 
embolic obstruction of the blood-vessels. 

Pathologic Anatomy. — Necrosis may be partial or total, 
and may occur in the center of the bone or at the periphery. The 
dead portion of the bone, termed sequestrum, presents itself as an 
irregular, more or less eroded fragment, almost completely or 
completely separated from the remaining structure. The separa- 
tion occurs by the process of demarcation, as in necrosis of the 
soft parts. This line consists of an area of absorption of the cal- 
careous matter and proliferation of the cellular elements. The 
necrotic portion, or sequestrum, acts as a foreign body, and by its 
continued irritation keeps up a suppurative inflammation of the 
surrounding tissues. Fistulous communication with the exterior 
is usually observed. If the sequestrum is peripheral and has 
been discharged, the periosteum or the bone may replace the lost 
tissue by regeneration. If the fragment is large or centrally 
placed, discharge is impossible and suppurative inflammation con- 
tinues, sometimes for years. In these cases considerable hyper- 
plastic material may be deposited over and around the sequestrum, 
and thus irregular thickening of the bone may be produced. 

A peculiar form of necrosis is that occurring in consequence of 
chronic phosphorus-poisoning. It is met with in persons engaged 
in the manufacture of phosphorus-matches, and affects the maxil- 
lary bone. The existence of carious teeth aids in the develop- 
ment of this form of necrosis, probably by admitting micro-organ- 
isms which infect the bone already altered by the poison. The 
process begins in the periosteal and subperiosteal portions of the 
bone, and ends in more or less complete necrosis. 

Associated Conditions. — Long-standing necrosis causes 
great deterioration of the general health, particularly in cases in 
which suppurating sinuses are formed. Systemic infections may 
follow and amyloid degeneration of various organs may occur. 

Osteomalacia. 

Definition. — This is probably a general disease leading to 
absorption of the bone-salts and to other changes in the bone, 
which cause extreme flexibility. 



712 



TEXT-BOOK OF PATHOLOGY. 



Etiology. — The causes of osteomalacia are still obscure. It 
is a disease occurring with especial frequency in puerperal women, 
but it may occur in men and in non-puerperal women. A number 
of theories have been offered to explain the disease, but none of 
them has been established. In some respects it seems not unlikely 
that it is a trophoneurosis. It is particularly frequent in certain 
regions (endemic), while in others it occurs very rarely (sporadic). 

Pathologic Anatomy. — The changes in the bone lead to 
various deformities and changes of appearance. Distortions, 
bends, and even fractures are observed in the long bones, and 
deformities due to abnormal curvatures of the spine are not infre- 
quent. The pelvis shows peculiar changes which may prove very 
troublesome during labor. The characteristic change is a beaked 
condition, due to displacement forward of the pubes and a lateral 
indentation. This gives a triangular form to the outlet of the pel- 
vis or superior strait. The bone-marrow is often quite red, and 
the periosteum in the neighborhood of bends or fractures may be 
thickened by cellular proliferation. The minute structure of the 
bone in osteomalacia shows a more or less pronounced absorption 
of calcareous matter, but the normal lamellar arrangement of 
the bone may be preserved. In the region of bends and fractures 
osteoid tissue of irregular structure, with bony corpuscles of con- 
siderable size, may be observed ; while in other situations the 
regular lamellar arrangement and the ordinary small-sized bone- 
corpuscles are seen. Irregular areas of homogeneous or granular 
appearance may be interspersed within the normal osseous tissues. 
The line of demarcation between such abnormal non-calcareous 
portions and the unaltered bone may be either sharply drawn or 
diffuse. 

Associated Conditions. — Patients suffering from osteo- 
malacia are usually greatly reduced or cachectic, and frequently 
perish with terminal pneumonia. Some cases end in recovery by 
restitution of the bone. It has been claimed that there is evidence 
in all cases of puerperal women of some bony absorption, and 
osteomalacia, therefore, would seem to be but an exaggeration of 
normal conditions. Normally the slight bony changes are cor- 
rected after the puerperal period is passed. 

INFECTIOUS DISEASES. 
Tuberculosis. 

Tuberculosis may occur in bones in several forms. Miliary 
tubercles may be found in the bone-marrow in the course of 
general miliary tuberculosis, and local tuberculous disease of the 
periosteum may be met with. The most frequent and most im- 
portant form of tuberculosis is tuberculous ostitis with caries. 



DISEASES OF THE BONES. 



713 



Etiology. — The involvement of the bones is nearly always 
secondary, the first manifestations of tuberculosis occurring in 
other structures, notably the lymphatic glands and the lungs. 
The original focus of disease is, however, frequently small, and 
may remain quiescent while the lesion in the bones advances. 
The disease of the bones may be due to direct extension or to 
hematogenous infection. Not rarely the joints are first involved 
and the neighboring bones only secondarily. 

Traumatic influences are of importance in determining the 
situation of hematogenous tuberculosis. The traumatism causes 
circulatory disturbances in the bone, and thus produces a suitable 
soil for the bacilli to find lodgement. Bone-tuberculosis is most 
frequent in early life ; it may actually begin in utero. 

Pathologic Anatomy. — The tuberculous lesion of bone first 
presents itself as an area of grayish color, with congestive redden- 
ing of the parts around and intense injection of the bone-marrow 
in its vicinity. Subsequently there are rapid cheesy change and 




Fig. 339.— Tuberculous caries of one of the bones of the foot : a, bony trabecula ; b, 
tubercle with caseous center; c, caseation in a focus of tuberculous tissue; d, giant-cells 
m tubercles ; e, osteoclasts ; /, fatty marrow (Kaufmann). 

more or less softening of the area of inflammation. Microscopically, 
tubercles in various stages of degeneration are discovered, and in 
addition areas of diffuse tuberculous granulation-tissue and caseous 
degeneration (Fig. 339). At the same time extension occurs at 
the periphery and new foci are established. The entire diseased 
area may be separated from the uninvolved bone as a sequestrum, 
but more frequently there is gradual carious softening, with forma- 
tion of semifluid, cheesy material containing gritty particles of 
bone or calcareous matter. Complete softening leads to the for- 



714 



TEXT-BOOK OF PATHOLOGY. 



mation of a "tuberculous abscess" (Fig. 340). In these cases 
a more or less irregular cavity is formed within the bone, 
the wall of the cavity being covered with a pyogenic membrane 
developed from the marrow and its extensions into the Haversian 
canals. The contents of the abscess are 
puriform or cheesy. The process tends to ex- 
tend to neighboring parts, particularly to the 
joints. When the abscess has penetrated the 
encasing bone it may spread within the soft 
parts, thus forming large tuberculous abscesses 
(so-called cold abscesses). These may burrow 
along the planes of the tissues to considerable 
distances from the point of formation, present- 
ing at the surface of the body in some favor- 
able situation, as, for example, in the groin, in 
psoas-abscesses. 

Reactive changes may occur locally, and 
more or less restitution may take place. Com- 
plete encapsulation of a small focus may occur 
by the formation of a surrounding zone of gran- 
ulation-tissue and cicatrization, or by new-for- 
mation of bone occurring after the activity 
of the tuberculous process has been arrested. 
"When adjacent portions of articulating bones 
are involved the integrity of the articulation 
is disturbed, and subsequently ankylosis may 
be established by the formation of exostoses 
and their union. 

Seats and Associated Conditions. — 
Among the bones more frequently affected are 
the vertebrae, the long bones, particularly the 
femur, and parts of the skull. In the vertebrae 
the bodies are generally affected, and angula- 
tion or distortion of the spine results (Pott's 
disease). The cold abscesses formed in these 
cases may burrow considerable distances, point- 
ing far below the place of origin. Those spring- 
ing from the cervical vertebrae may point be- 
neath the mucous membrane of the pharynx or 
esophagus, or anteriorly in the neck above the 
clavicle or shoulder. The abscesses formed 
in tuberculous caries of the dorsal vertebrae may point under Pou- 
part's ligament. Tuberculous disease of the petrous portion of 
the temporal bone is not infrequent following tuberculous disease 
of the ear ; it is important as a possible cause of tuberculous men- 
ingitis. Tuberculosis of the head of the femur and of the hip- 
joint is one of the most frequent forms of surgical disease in chil- 



Fig. 340.— Tubercu- 
lous " abscess " in the 
lower end of the hume- 
rus (modified from Bol- 
linger). 



DISEASES OF THE BONES. 



715 



dren. The phalanges are sometimes involved in early childhood 
by a curious form of tuberculosis, in which the shaft of the bone 
increases in size by gradual absorption and tuberculous softening 
within and deposition of new bone from the periosteum without. 

Syphilis. 

Syphilitic disease of bones may appear in various forms. Allu- 
sion has already been made to the condensation of the bones, or 
osteosclerosis, in this disease. Syphilis may also occur in the peri- 
osteum as a nodular periostitis, or in the substance of the bone in 
the form of degenerating gummata. Congenital syphilis gives rise 
to certain peculiar alterations. 

Etiology. — Syphilitic changes in bone are confined almost 
exclusively to the tertiary period. They may occur without other 
luetic disease, or as concomitants of hepatic, splenic, or other vis- 
ceral disorders. The disease of the bones is frequently determined 
by local injuries ; especially is this true of the periosteal forms. 

Pathologic Anatomy. — Syphilitic periostitis is very common 
upon the shin-bone, less frequent in the periosteum of other long 
bones. There is, first, slight swelling of the periosteum, due to 
multiplication of the cells. Subsequently this cellular mass 
undergoes gummy or mucous degeneration, and the mass presents 
the appearance of a small gumma. Superficial erosion, or even 
necrosis, of the bone may take place, and discharge of the con- 
tents may occur. Following this, hypertrophic processes in the 
bone and adjacent periosteum lead to the formation of bony nodes. 
These nodes may, however, be formed without the occurrence of 
softening and discharge from the periosteal lesion, the process in 
this case being one of simple ossifying periostitis. Gummata of 
the bones generally begin in the deeper layers of the periosteum, 
but tend to involve the bone more extensively than the form just 
described. The gummatous infiltration and proliferation occur 
along the blood-vessels of the periosteum and extend into the sub- 
stance of the bone. Considerable areas may thus be implicated. 
The bone itself is absorbed, or may undergo rapid caries or 
necrosis. Around the area of syphilitic change may occur a 
zone of reactive hyperplasia of the bone and periosteum. The 
gummata themselves become cheesy or undergo mucoid degenera- 
tion, and eventually may discharge upon the surface. Syphilitic 
gummata are most frequent in the bones of the head, tibia, and 
sternum. 

Occasionally gummata arise in the marrow of the bones instead 
of the periosteum. 

Congenital Syphilis. — The bony changes of congenital syphilis 
are quite characteristic. The alterations occur at the junction of 
the epiphyses with the diaphyses of the long bones. Longitudinal 



716 



TEXT-BOOK OF PATHOLOGY. 



section through these parts shows the line of junction as a bluish- 
white or yellowish-white irregular zone about 2 or 3 mm. in thick- 
ness (Plate 7). In more advanced stages this line becomes thicker 
and more yellow. The minute changes consist in proliferation of 
the cartilage-cells and subsequent fatty degeneration. Microscopi- 
cally the proliferated cellular elements, fatty cells, and granular 
detritus are conspicuous features. The epiphyses may be com- 
pletely separated from the shaft. 

Associated Conditions. — Involvement of the neighboring 
parts is not infrequently seen in syphilitic diseases of the bones ; 
thus there may be gummatous infiltration of the superficial tissues 
with syphilis of the bones of the extremities, while in the case 
of skull-bones extension inward may lead to involvement of the 
dura and brain. When the process occurs about the foramina 
of exit of nerves the sheaths of the latter may become involved. 
Gummata of the sternum sometimes lead to the formation of retro- 
sternal collections of puriform material. Amyloid degeneration 
of various organs frequently follows bone-syphilis. 

Lepra. 

Changes may occur in the bones in cases of mutilating leprosy, 
or more rarely in nervous lepra. Among these changes are ostitis 
and osteomyelitis ; considerable destruction of the bones may be 
produced. 

TUMORS. 

Exostoses are frequently met with in connection with defi- 
nite disease of the bones and joints, or as more or less idiopathic 
outgrowths (Fig. 44). They may be cartilaginous or fibrous in 
character, but subsequently may become osseous. They present 
themselves as flat, rounded elevations, or as more or less irreg- 
ular outgrowths. Sometimes they are multiple and involve a 
number of bones of the skeleton. In such cases, particularly, 
heredity has been claimed as an important cause. 

Fibroma, lipoma, myxoma, and angioma may be men- 
tioned among the true tumors as benign growths occasionally met 
with. They arise most frequently from the periosteum. 

Chondroma and osteoma are more common than these, and 
involve any part of the bone (Figs. 42 and 45). 

Sarcoma. — The most important of the primary tumors of 
bone is sarcoma. This may originate in the periosteum, bone- 
marrow, or the bone itself. It may be spindle-celled, or less fre- 
quently round-celled or alveolar. Sometimes it is melanotic. The 
giant-cell sarcoma, or osteosarcoma, is particularly important. 
It is most frequently met with in the lower jaw, beginning within 
the bone and causing a more or less rapid swelling. The tumor 
is surrounded by a shell of bone, which, however, sooner or later 



Plate 7. 




Epiphyseal junction in congenital syphilis ; section stained with hematoxylin. 



DISEASES OF THE BONES. 



717 



becomes perforated when the new growth spreads to the neighbor- 
ing parts (Fig. 58). In all forms of sarcoma there is absorption of 
the bone-substance in the vicinity. A form of sarcoma springing 
from the periosteum is described under the name of osteoid sar- 
coma. This tumor consists of fibromatous or round-celled sarcom- 
atous tissue in which osteoid elements are irregularly embedded. 
More or less calcification and bone-formation are observed. The 
tumor may be quite soft or very hard ; it tends to spread to the 
neighboring soft parts, and may give rise to metastasis. It is 
particularly frequent at the ends of the long bones. 

Secondary sarcoma of the bone-marrow is not rare in gen- 
eral sarcomatosis. 

Myeloma. — This term has been applied to a form of multiple 
primary tumor of the bone-marrow allied to the lymphatic growths 
of leukemia and Hodgkin's disease. The term lymphadenia ossea 
has also been given to it. Probably a number of distinct condi- 
tions (some of them secondary tumors) have been described under 
these names. 

Chloroma is a form of sarcoma, having a greenish or yellow- 
ish color, that is met with in the periosteum, especially about the 
orbits and other parts of the skull. 

Primary carcinoma of the bones has been observed in a 
few cases. It can only be explained upon the assumption that 
islets of epithelial tissue have been deposited in the bone by faulty 
development. Most cases, however, described as primary carci- 
noma were probably in reality alveolar sarcomata. 

Secondary carcinoma of the bones is not rarely met with, 
especially in cases of cancer of the breast, thyroid gland, and 
prostate. The secondary nodules may occupy the periosteum or 
the bone-marrow. The bone becomes exceedingly fragile, and 
fractures are not infrequent. 

Cysts and Parasites. — Cystic transformation of myxomata 
and of sarcomata may be met with. Occasionally dermoid cysts 
are observed. Among the parasitic diseases Cysticercus cellulosse 
has been described in a number of instances. 



718 



TEXT-BOOK OF PATHOLOGY. 



CHAPTEE X. 

DISEASES OF THE JOINTS. 

Iytlxation. — The most frequent injury of joints is that known 
as luxation, in which the relations of articulating bones are dis- 
turbed. In these cases the ligaments and other soft tissues around 
the joints are more or less torn, and in consequence become in- 
flamed. If the luxation is reduced, this inflammation subsides 
quickly, and frequently normal conditions are restored. If the 
luxation persists, various secondary changes may occur. Anky- 
losis in abnormal positions may take place by the formation of 
fibrous adhesions, or in more favorable cases a false joint may be 
established. In the latter cases local atrophy takes place in one 
of the bones, forming a depression into which the end of the other 
fits. Later, ossifying periostitis produces an elevation around the 
depression of the socket, and thus a well-formed joint may be 
produced. 

Ankylosis is the term applied to the condition in which the 
normal movability between articulating bones is prevented by in- 
terosseous attachments. Pathologically, ankylosis may be fibrous, 
cartilaginous, or bony. All of these forms are met with after 
chronic inflammatory conditions of the joints. 

DISTORTIONS OF JOINTS. 

Distorted conditions of the joints may be due to contractions 
of the muscles and tendons, or to cicatricial tissue in the neigh- 
borhood of the articulation. Changes in the joints themselves 
may be present as primary or as secondary conditions. Among 
the more important of such deformities of joints are the various 
sorts of club-foot : pes varus, the sole of the foot turned in ; 
pes valgus, the sole of the foot turned out ; pes equinus, the foot 
extended and supported upon the anterior ends of the metatarsal 
bones ; pes calcaneus, the foot flexed and resting on the heel. 
Combinations of these conditions are frequently met with. At 
the knee-joint are found : genu valgum, in which the knees are 
bent in (knock-knee), and genu varum, in which the knees are 
bent out (bow-legs). 

CIRCULATORY DISTURBANCES. 

Hyperemia of the joints occurs as a part of acute inflamma- 
tions, and involves the synovial membranes particularly. The 
synovial fluid may be increased in quantity. 

Hemorrhage into the joint may result from traumatic causes 
or from inflammatory conditions, particularly in the course of hem- 



DISEASES OF THE JOINTS. 



719 



orrhagic diseases, notably scurvy and hemophilia. The blood may 
remain fluid for a long time, and the joint not rarely has the ap- 
pearance of chronic arthritis with effusion. Later, resorption of 
the blood takes place. 

Dropsy of the joints occurs in the course of acute and chronic 
inflammations. 

INFLAMMATIONS. 

Acute arthritis may be traumatic or hematogenous, or in 
other cases is secondary to disease in the vicinity. Hematogenous 
arthritis may occur in the course of various infectious diseases, 
such as scarlet fever, small-pox, pyemia, etc. In the same group 
must be considered acute articular rheumatism, which is doubtless 
an infection conveyed to the joint through the blood. 

Pathologic Anatomy. — Various forms may be distinguished, 
such as the dry or fibrinous, the serous, and the seropurident. In 
all cases there is, first, a deep congestion of the synovial mem- 
brane. The ligaments and the cartilage are more or less impli- 
cated at the same time. The terms synovitis, implying involve- 
ment of the synovial membrane, and panarthritis, implying gen- 
eral involvement, may be applied. In the dry or fibrinous form 
there is a deposit of fibrin upon the surface, with or without serous 
exudation. In the genuine serous form the exudation is purely ser- 
ous, but more commonly seropurulent liquid is observed. Entirely 
purulent exudate is sometimes formed (empyema of the joints). 

Results. — In the milder cases complete resolution may take 
place without destruction of the tissues of the joint. In the more 
serious cases there is inflammation of the articulating cartilages, 
with consequent ulceration or caries, or even considerable necro- 
sis, of the cartilage. The underlying bone may be laid bare, and 
ostitis or osteomyelitis may result. Sometimes discharge of 
purulent material into the surrounding tissues occurs, and fistulous 
communications with the exterior may be established. These 
processes may lead to extensive disorganization of the joints, with 
luxations and, in later stages, ankylosis. 

Associated Conditions. — General systemic infection may follow 
these acute inflammations of the joints. 

Chronic arthritis may be due to a variety of causes. It 
may follow the acute forms already described or may be primarily 
chronic. Among the more important causes are traumatism and 
certain infections. It occurs in the course of gout and in certain 
nervous diseases, probably as the result of disturbance of the 
trophic mechanism. Chronic arthritis of the aged has perhaps a 
similar causation, and rheumatoid arthritis is nearly allied. 

Pathologic Anatomy. — A variety of forms may be distinguished. 
The same etiologic factors may, however, give rise to one or 
another in individual cases. 



720 



TEXT-BOOK OF PATHOLOGY. 



Chronic serous arthritis, or hydrops articulorum, is fre- 
quently due to repeated acute arthritis. The joint is filled with thin 
synovia ; and the synovial membrane is somewhat thickened. The 
surface of the joint may be more or less covered with an injected 
synovial membrane (synovitis pannosa). The knee-joint is most 
frequently involved. 

Chronic purulent arthritis is always infectious, and is usually 
the outcome of an acute seropurulent or purulent arthritis. The 

conditions met with have already 
been described. It terminates in 
more or less extensive disorganiza- 
tion of the joint, and in favorable 
cases in fibrous ankylosis (Fig. 341). 

Arthritis deformans, or rheuma- 
toid arthritis, occurs in persons past 
middle age, but sometimes in young 
persons, and even in childhood. Con- 
stitutional depression and exposure 
seem in some way to predispose. 
There are, first, alterations in the 
cartilages of the joints, consisting 
of softening and ulceration or ero- 
sion, which make the surface irreg- 
ular and rough. At the same time 
some hyperplasia of the cartilage- 
cells takes place, but the hyperplas- 
tic elements subsequently undergo 
degeneration, and are absorbed. In 
this way the cartilage is gradually 
reduced and the ends of the bone 
laid bare. The synovial membrane 
and ligaments at the same time become thickened by hyperplasia. 
Subsequently the articulating end of the bone is involved. There 
is, first, absorption, and secondarily proliferative changes at the 
periphery of the articulation, in the form of exostoses or osteo- 
phytes. The joint is considerably deformed and thickened. Sub- 
luxations are common, and the deformity leads to immobility of 
the joint, or ankylosis. This form of arthritis is particularly 
common in the metacarpophalangeal joints of the hand, and in 
the other small joints of the hands and feet (Fig. 342). Later 
the knee, elbow, and vertebral articulations may be involved. 

Chronic dry arthritis with ulceration, or senile arthritis, is 
particularly common in the hip-joint (malum coxaz senile). There 
is gradual absorption of the cartilages and of the exposed surfaces 
of the bone. Subsequently the surrounding parts of the bone 
undergo sclerosis and hypoplasia. The changes are similar to 
those of rheumatoid arthritis, but are more slowly developed. 




Fig. 341.— Fibrous ankylosis, due to 
chronic purulent arthritis. 



DISEASES OF THE JOINTS. 



721 






Fig. 342.— Rheumatoid arthritis, showing extensive deformity of the hands. 

Neuropathic arthritis is met with in the course of spinal dis- 
eases, such as locomotor ataxia and syringomyelia (Fig. 343). It re- 




Fig. 343— Neuropathic arthritis of the knee in a case of locomotor ataxia (case of Dr. C. 

W. Burr). 

sembles the forms just described, is slowly developed, and is usually 
quite painless, suggesting a purely degenerative or trophic disorder. 

46 



722 



TEXT-BOOK OF PATHOLOGY. 



Gouty Arthritis. — Gout is a constitutional disease with a 
tendency to a peculiar form of arthritis. The latter consists in 
the deposit of crystals of urate of sodium and calcium in the carti- 
lage-cells and intercellular substance of the articulations, and in 
more advanced cases in the connective tissue of the joints and the 
tissues round the joints (Fig. 344). These crystalline deposits occur 




Fig. 344.— Deposit of crystals of urate of sodium in an articular cartilage (Lancereaux). 

in definite attacks, as a rule, each attack (gouty paroxysm) being 
marked by inflammatory processes in the joint. Hyperemia of the 
synovial membrane, with serous effusions and with sometimes more 
evident inflammatory manifestations (hyperplasia of the cartilage- 
cells and round-cell infiltration), is observed during the parox- 
ysms, and by their repetition chronic changes in the joint are 
produced. The cartilages may become more or less eroded, and 
even carious changes and suppuration may take place. The joints 
most frequently involved are the small joints of the hands and 
feet, notably the metatarso-phalangeal joint of the great toe. The 
larger articulations are less commonly involved, and usually after 
the smaller joints. 

Associated Conditions. — The pathology of gout is by no means 
confined to the changes in the joints. The disease is a general 
one, and pathologic changes are found in various organs. There 
is a tendency to thickening of the blood-vessels, to atheroma, and 
to sclerotic changes in the kidney, liver, and heart ; and uratic 
deposits may occur in the organs named or in the subcutaneous 
tissue or superficial cartilages, such as those of the ear and nose 
(gouty tophi). Concretions or calculi are frequently formed in the 
kidney or bladder. 

INFECTIOUS DISEASES. 
Tuberculosis. 

Tuberculosis, when primary in the joints, usually begins in the 
synovial membrane. Frequently it is secondary to tuberculosis 
of the adjacent bone. In such cases any part of the joint may be 
first involved. 



DISEASES OF THE JOINTS. 



723 



Etiology. — Tuberculous arthritis is most frequent in child- 
hood, and occurs in those predisposed by heredity. The immedi- 
ate determining cause may be traumatism, this serving to localize 
the disease in a joint rendered peculiarly susceptible. Tubercu- 
lous arthritis is frequently secondary to scrofulous disease of the 
skin or glands, or to pulmonary tuberculosis, but is often primary. 

Pathologic Anatomy. — The changes met with in the joints 
vary somewhat in different cases. In instances beginning in the 
synovial membrane there are formed more or less abundant, soft, 
spongy granulations, which may eventually fill the entire joint- 
cavity. These are pinkish or whitish in color, and may show 
gray or yellow spots or tubercles quite plainly. Later this granu- 
lation-tissue tends to degenerate, becoming mucoid or breaking 
down by suppurative or cheesy change. In the early stages the 
soft tissues of the joint are considerably inflamed and edematous ; 
later they may show ulcerative or necrotic change, and similar 
alteration may occur in the articular cartilages. Puriform soften- 
ing of the granulations and the tissues of the joint may lead to the 
development of cold abscesses within the joint, and the latter may 
eventually burrow to the exterior. In cases progressing unfavor- 
ably the joint is greatly disorganized by the advancing necrotic 
changes. The abnormal productions are either discharged or in- 
spissated, and ankylosis of the joint by fibrous adhesions takes place. 

The external appearances of tuberculous joints are often quite 
distinctive. The joint is swollen and boggy, or somewhat elastic 
to the touch, and usually more or less distorted from subluxation. 
There is little evidence of acute inflammation. In cases termi- 
nating in ankylosis the bones are generally left in faulty position 
in consequence of the formation of adhesions and the irregular 
contractions of muscles. 

Secondary Disorders. — Long-standing tuberculosis of the 
joints occasions profound disturbances of the general health, and 
sometimes causes definite disease, such as amyloid degeneration of 
various organs. Disseminated tuberculosis rarely results. 

Syphilis. 

Syphilitic disease of the joints may occur in hereditary lues. 
The cartilages of the joints are eroded, and thickening of the 
ligaments with puriform exudation into the joint is observed. 
The phalangeal articulations are most frequently involved. In 
later life gummata in the neighborhood of the joints may invade 
the latter by contiguity. 

TUMORS. 

Hyperplastic conditions are met with in the synovial fringes 
of the joints in association with arthritis or independent of such. 



724 



TEXT-BOOK OF PATHOLOGY. 



These hyperplasias may take the form of fibrous growths, or they 
may become iipomatous. An interesting form of new growth is 
seen in the so-called rice-bodies. These are small fibrous or carti- 
laginous bodies, up to the size of a small nut, which are entirely 
free in the joint or attached by a fine pedicle to the synovial mem- 
brane. They are formed from the synovial fringes, and probably 
result from injury in most cases. The joints may be secondarily 
involved in various forms of bony tumors. 

THE TENDON=SHEATHS AND BURS^E. 

Inflammations of the sheaths of tendons (tenosynovitis) and 
of the bursse (bursitis) occur under similar circumstances and in 
similar forms as inflammations of the joints. A form of chronic 
bursitis with dropsical effusion frequently occurs in the bursa 
beneath the patella from chronic irritation (housemaid's knee), and 
in the bursa at the joint of the elbow (miner's elbow). These 
conditions are analogous to hydrops articulorum. 

Ganglion is a condition of the tendon-sheaths of some clinical 
interest. It presents itself as a rounded cystic nodule, most fre- 
quently upon the back of the hands and wrists. Distinct fluctua- 
tion may be discovered, or the cyst may be so dense that it feels 
stony hard. The ganglion results from a localized dropsical con- 
dition of the sheath of the tendons, with frequently a lateral 
hernious projection. A similar condition is sometimes caused by 
projection of the synovial membrane of the joints. 



CHAPTER XI. 

DISEASES OF THE VOLUNTARY MUSCLES. 

Congenital malformations are occasionally met with, such 
as absence of a part or of an entire muscle. 

HYPERTROPHY. 

Hypertrophy is frequently produced by athletic exercise or 
laborious occupations. This affects the parts brought into play, 
and is proportioned to the amount of work and the constitution or 
condition of the individual. The muscle-fibers increase in thick- 
ness and probably also in number. 

Sometimes muscular hypertrophy is met with in cases in which 
no adequate cause is discoverable. Thus in local or general giant 
growths the muscles may be involved with other parts. 

Pseudohypertrophy will be discussed among the degenerative 
conditions. 



DISEASES OF THE VOLUNTARY MUSCLES. 



725 



CIRCULATORY DISTURBANCES. 

Anemia of the muscles may be part of a local or general 
anemia ; it is often quite insignificant in comparison with anemia 
of other parts. In some of the general anemias the muscles may 
present a dark appearance, due to degenerative conditions. 

Hyperemia is physiologic during and after exercise. It 
occurs as an active process in association with inflammatory con- 
ditions and as a passive congestion in cases of vascular stasis. 

Hemorrhages may be traumatic, or may result from rupture 
of the vessels in consequence of inordinate blood-pressure or local 
degeneration of the vessel- walls and the surrounding muscle-fibers. 
Among the conditions in which hemorrhage takes place are tetanus 
and other convulsive disorders, fevers, and hemorrhagic diseases, 
such as scurvy, hemophilia, and septic diseases. The hemorrhages 
may occur in the form of small extravasations between the fibers, 
or of more extensive infiltrations in the intermuscular planes. In 
cases of traumatism, scurvy, or hemophilia, considerable blood- 
tumors may be formed, the muscle-fibers being pushed aside or 
torn apart. The blood is more or less rapidly absorbed. Pigmen- 
tation and fibrous-tissue proliferation may result. 

Embolism of the arteries or thrombosis of the veins does 
not produce serious disturbances, as a rule. In cases of embolism, 
secondary results may follow if the embolism is infective. 

INFLAMMATIONS. 

Inflammation of the muscles, or myositis, may be acute 
or chronic, and may present itself in a variety of forms. Acute 
myositis may be local or disseminated. 

localised Acute Myositis. — This form may be due to 
injuries, such as contusions of the muscles or wounds communi- 
cating with them, or may be infectious in character, resulting from 
the direct extension of infectious diseases of the skin, subcutaneous 
tissues, bones, and other adjacent parts, or from embolism. A 
serous, a hemorrhagic, and a purulent form may be distinguished. 

Serous myositis is characterized by an edematous condition of 
the muscle, which gives it a peculiar gelatinous appearance on 
section. Microscopically there is cellular infiltration of the mus- 
cle-bundles, while the muscle-fibers themselves become swollen 
and suffer granular degeneration or hyaline change, and some- 
times vacuolation. 

Hemorrhagic myositis is an intense form, and is met with in 
muscles adjacent to gangrenous or phlegmonous lesions, malignant 
pustules, and the like. Myositis occurring in scorbutic individuals 
is frequently of the hemorrhagic form, as is also that which occurs 
in consequence of the sting of venomous snakes or other animals. 



726 



TEXT-BOOK OF PATHOLOGY. 



The muscle becomes more or less tensely swollen, and on section 
the hemorrhagic infiltration is plainly visible as a diffuse process 
or as localized areas of hemorrhage. 

Suppurative myositis may be circumscribed or diffuse. Circum- 
scribed myositis, or abscess of the muscle, may result from entrance 
of micro-organisms through the lymphatic or vascular circulation, 
or it may be due to traumatism, with communications from the 
surface. Occasionally suppurative inflammation occurs in an ob- 
scure manner, when the term cryptogenetic myositis is applicable. 
Distinctly metastatic abscesses may be occasioned by embolism. 

In association with suppurative inflammations of the skin or sub- 
cutaneous tissues and the mucous membranes there may be sero- 
purulent or phlegmonous myositis, with the formation of irregular 
abscesses. In these cases the lesion spreads by infiltration, and 
the muscle-fibers undergo widespread degeneration (fatty degenera- 
tion, hyaline change, and necrosis). Abscesses in the muscles ex- 
tend and rupture in various directions, and may leave consider- 
able areas of scar-formation. 

Disseminated acute myositis or polymyositis may ap- 
pear without any definite cause, sometimes in association with 
tuberculosis of the lungs, or as a distinctly secondary affection in 
association with infectious diseases, like typhoid fever, diphtheria, 
etc. In the primary form there may be widespread muscular dis- 
ease, with swelling and tenderness of the muscles and sometimes 
redness and edema of the skin. The term pseudotrichinosis was 
applied from the resemblance of the appearances to those of trichi- 
nosis, and the name dermatomyositis has also been given this con- 
dition. Some of the conditions included under the heading mus- 
cular rheumatism by clinicians are doubtless instances of the kind 
here referred to. Examination of the muscles shows pallor of the 
tissue, and sometimes visible areas of degeneration. Microscopi- 
cally there are cellular infiltration between the muscle-fibers and 
swelling, with loss of striation of the fibers themselves. More 
advanced degenerations of the fibers, such as granular change, 
coagulation-necrosis, and vacuolation, may be observed. The 
affected muscles lose their functional contractile power, and more 
or less palsy results. When affecting the muscles of the pharynx 
and respiration this becomes serious in predisposing to inspiration- 
pneumonias. 

The condition described as secondary acute polymyositis is 
degenerative to a greater extent than inflammatory, and will be 
considered among the degenerations. 

Chronic myositis may be suppurative in type or produc- 
tive. 

Chronic suppurative myositis may be the outcome of acute sup- 
puration, and is particularly frequent in association with tubercu- 
losis and actinomycosis. 



DISEASES OF THE VOLUNTARY MUSCLES 727 

Chronic productive myositis is characterized by the formation of 
connective tissue between the muscle-fibers. The fibers them- 
selves, as a rule, undergo degenerative changes, though occasion- 
ally snowing regeneration to some extent. This condition may be 
the termination of acute myositis, or it may occur in the vicinity 
of various localized diseases of the muscles or of the neighbor- 
ing parts. In some cases, if not all, the primary change is 
degeneration of the muscle-fibers, and the interstitial or fibrous 
tissue is reactive in character. Some of the cases will be con- 
sidered under the head of muscular atrophies. The changes 
that occur in the interstitial tissue of the muscles consist pri- 
marily of proliferation and round-celled infiltration. Later there 
is formation of firm connective tissue. Some multiplication of 
the muscle-nuclei and actual increase in size of the muscle- 
fibers may be observed. Degeneration of the muscle-fibers, 
however, is more prominent, and is generally in proportion to 
the degree of connective-tissue change. The fibers may show 
cloudy swelling or hyaline changes, or more complete degenera- 
tion, such as fatty degeneration, fragmentation, or vacuole-forma- 
tion. 

Ossifying- myositis is a variety of productive myositis. It may 
occur in the form of bony nodules in parts subjected to constant 
irritation or strain, as in the case of the deltoid muscle in soldiers 
and the adductor muscles in horsemen. Similarly, in the vicinity 
of disease of the bones and periosteum, nodules may develop in 
the muscle. A form of more general disease, termed myositis 
ossificans progressiva, has been observed in youthful persons, with- 
out discoverable cause. It affects the muscles of the back and 
neck, and sometimes those of all parts of the body. The muscles 
are swollen, and first present inflammatory manifestations, termi- 
nating in fibrous change which finally leads to bone-formation. 
The osseous tissue is at first in the form of spicules or small 
nodules, but gradually increases to considerable proportions. The 
muscles themselves contract, and various deformities with pseudo- 
ankyloses may result. The muscles of the face, diaphragm, and 
heart are unaffected. 

ATROPHY AND DEGENERATIONS. 

Several forms of atrophy are recognized. Certain cases are 
dependent upon disease of the spinal cord or nerves (neuropathic 
form), others occur as primary diseases of muscles (myopathic 
form), and in another group the change is due to simple nutritional 
processes (simple and senile forms). 

Neuropathic muscular atrophy may be the result of dis- 
ease of the anterior horns of the gray matter of the cord. To the 
cases in which this lesion is the underlying pathologic condition the 



728 



TEXT-BOOK OF PATHOLOGY. 



term progressive muscular atrophy has been applied. The causes 
of this disease are obscure. 

It leads to progressive atrophy of the muscles of the hands, 
arms, and shoulders, and less frequently of those of the body and 
buttocks. It usually begins in the small muscles of the hands, 
but sometimes affects those of the shoulders first. The muscles 
become pale and rather flabby. Microscopically the fibers show 
various forms of degeneration. Fragmentation in a longitu- 
dinal or in a transverse direction, coagulation-necrosis, and occa- 
sionally fatty degeneration of the fibers may be seen. Sometimes 
the fibers seem to grow smaller by a simple" atrophic process (Fig. 
345). Coincidently, reactive proliferation is seen in the connective 




Fig. 345.— Neuropathic muscular atrophy, showing atrophy of the muscle-fibers, increase 
in the interfascicular fibrous tissue, and thickening of the blood-vessel walls. 

tissue between fibers, and doubtless this to some extent causes 
further muscular degeneration. The muscle-cells themselves may 
proliferate quite extensively. 

Secondary neuropathic muscular atrophies may occur in various 
spinal diseases, such as syringomyelia and in degenerations follow- 
ing cerebral disease. These are essentially similar in character to 
the primary neuropathic variety, though their clinical character is 
different. Section, disease, or injury of motor nerves may lead to 
local atrophies by separating the muscles from their trophic cen- 
ters in the cord. 

Myopathic muscular atrophy occurs in children and young 
persons, and is frequently hereditary. It begins in the buttocks, 
thighs, or calves, and sometimes in the shoulders. Two forms 
have been distinguished : the simple atrophic form and the pseudo- 
hypertrophic form. The anatomical changes in the former are 
the same as in the neuropathic variety just described. 



DISEASES OF THE VOLUNTARY MUSCLES. 729 



Pseudohypertrophic Muscular Atrophy. — In this condition the 
muscles increase greatly in size, but are soft and flabby. The 
child may present the appearance of an athlete, with enormous 
calves and thighs, but is extremely weak and can scarcely stand. 
Microscopically the causation of the enlargement is found to be a 
considerable degree of intermuscular proliferation of connective 
tissue, with marked fatty infiltration. Sometimes in this form, as 
well as in other varieties, some actual enlargement of the muscle- 
fibers is observed, but this is doubtless degenerative. 

Simple muscular atrophy may be senile in origin or due to 
lack of exercise. In these cases the muscle-fibers become smaller, 
and some proliferation of the connective tissue is generally present. 
In senile cases brown atrophy may occur, brownish pigment- 
particles being deposited in the atrophic fibers, especially near the 
nuclei. 

Parenchymatous degeneration of the muscles may occur 
in the vicinity of inflammatory lesions, tumors, or other areas of 
disease. It may also occur in the course of infectious diseases in 
association with coagulation-necrosis. The fibers become cloudy 
and lose their striated appearance from the presence of minute 
granules. In some instances inflammatory changes in the inter- 
fascicular connective tissues are associated with the degeneration 
of the fibers. Cases of this sort may be called secondary acute 
polymyositis. 

Patty degeneration is found under the same circumstances 
as the above, and also in chronic cachectic diseases and in cases 
of poisoning with phosphorus and other "parenchyma-poisons." 
The muscle-fibers have a streaked or spotted, yellowish appear- 
ance, and are more or less flabby. Microscopically the fibers are 
seen to be filled with small oil-droplets, which obscure the stria- 
tums. All parts of the fiber may become degenerated until the 
sarcolemma-sheath contains only a mass of fat-droplets and 
detritus. 

Patty infiltration may occur in association with atrophy in 
the condition above described — pseudohypertrophic muscular 
atrophy ; and in various nervous diseases in which the muscles 
waste from disease or trophic change. A certain amount of 
lipomatosis may occur in general obesity. 

Amyloid degeneration is rare and unimportant. 

Calcification may occur in the form of ossifying myositis, 
and locally in scars following various local diseases — abscesses, 
etc. 

Coagulation-necrosis, or hyaline degeneration, is of 

great clinical importance. It was first discovered by v. Zenker 
as one of the lesions occurring in typhoid fever. The muscle- 
fibers at first become granular and cloudy {parenchymatous degen- 
eration), and later waxy or hyaline change occurs in streaks or 



730 



TEXT-BOOK OF PATHOLOGY. 



completely transforming the fibers. Transverse fragmentation is 
common, and gross rupture of the muscle may be met with. In 
the latter cases hemorrhagic infiltration, or even considerable 
hemorrhage (hematoma), may be occasioned. Reactive inflam- 
matory change in the interstitial connective tissue is generally 
present. This disease occurs in the course of typhoid fever, but 
also in various other febrile and infectious conditions. It is most 
common in the abdominal muscles (rectus abdominis), in certain 
muscles of the extremities, and in the heart. The latter situation 
is, of course, of greatest significance (see Diseases of the Heart). 

INFECTIOUS DISEASES. 

Tuberculosis may occur in the form of cold abscesses in 
association with tuberculous disease of bone, or less frequently of 
the lymphatic glands or other parts. In these cases there is a 
gradual extension of the caseous and liquefying tuberculous dis- 
ease into the muscles, and sometimes the abscesses burrow to 
great distances within the muscular sheath, as, for example, in 
psoas abscess. Less destructive tuberculous myositis may occur 
in the muscles beneath the skin and mucous membranes by exten- 
sion of tuberculous processes. In these cases cellular infiltration 
and tubercle-formation, with some caseous change, may be observed. 
Miliary tubercles, or larger tubercular nodules due to hematogenous 
infection, are rare. 

Syphilis may occur in the form of gummata, and it is likely 
that some cases of diffuse productive myositis are syphilitic in 
nature. As in other parts of the body, the blood-vessels in these 
cases have been described as particularly thickened. 

Glanders, actinomycosis, and anthrax may involve the 
muscles in the vicinity of the specific lesions. Nodular and, later, 
necrotic or suppurative foci are the lesions observed. 

TUMORS AND PARASITES. 

The tumors of muscles, for the most part, spring from the 
interstitial connective tissue. Among the benign tumors fibromata, 
myxomata, and lipomata are sometimes met with. Osteoma and 
chondroma are found as localized lesions resulting from irritation 
or as true tumors. Striped muscle-tumors, or rhabdomyomata, 
are rarely found in the muscles, though occasionally seen as small 
nodules. 

More important than the above is sarcoma, w T hich occurs as 
a primary tumor comparatively frequently. The fibrous and 
spindle-celled varieties are common, and round-celled sarcoma are 
sometimes observed. The tumors originate from the connective 
tissue, though it is held by some that the muscle-fibers themselves 
may undergo sarcomatous transformation. 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 731 



Carcinoma is a rare tumor, and is always secondary. The 
secondary form is not rarely seen in the muscles in the vicinity of 
carcinomata of other structures, such as the mammary gland. 

Among the parasitic diseases of muscles may be mentioned 
trichinosis, cysticercus invasion, and hydatid disease. The first 
occasions disseminated myositis, to which reference has already 
been made. The other two conditions are rare and not important. 



CHAPTER XII. 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 

THE DURA MATER. 

CIRCULATORY DISTURBANCES. 

Active hyperemia occurs in the dura in association with 
tumors, gumma ta, and other focal diseases. The vessels of the 
dura surrounding the area of disease become distended and the 
membrane may be diffusely reddened. 

Passive hyperemia may occur under the same circumstances 
as the above, and also in cases of thrombosis of the venous sinuses. 

Hemorrhages are usually due to traumatism, and may occur 
on the outer or inner surface of the dura. Extradural hemor- 
rhages are more common than intradural, especially in oases in 
which there is fracture of the skull. A collection of blood be- 
tween the skull and the dura is sometimes designated internal 
cephalhematoma. Small hemorrhages into the dura may occur in 
infectious or hemorrhagic diseases and in cases of death from 
asphyxia. 

INFLAMMATIONS. 

Inflammation of the dura, or pachymeningitis, may be 

acute or chronic, and hemorrhagic, suppurative, or productive in 
character. 

Hemorrhagic pachymeningitis occurs more frequently in the aged 
than in the young, and is not uncommon in the insane. Chronic 
alcoholism and traumatism seem to be etiologic factors of some 
importance. In the early stages of the disease the inner surface 
of the dura exhibits a superficial deposit or membrane of grayish 
color, with brown or red spots, the former being composed of 
altered blood-pigment (hematoidin). Often several layers are 
present, indicating successive exacerbations. Microscopically the 
membranous deposit is found to consist of soft granulation-tissue 



732 



TEXT-BOOK OF PATHOLOGY. 



containing numerous thin-walled blood-vessels. Later, diapedesis 
of blood-corpuscles, or actual hemorrhages, occur, and the dis- 
eased area may have the appearances of a simple collection of blood 
or of a more or less stratified hemorrhagic exudate. Sometimes 
the amount of exudate and of hemorrhage may be such as to cause 
considerable cerebral compression, and in other cases death may 
occur from the hemorrhage itself. Occasionally the blood is in 
part absorbed, and a serous collection (hygroma durce matris) 
results. The seat of the disease is usually in the area of distri- 
bution of the middle meningeal artery. 

Suppurative pachymeningitis may occur in consequence of 
injuries, caries, or other diseases of the skull. Sometimes it re- 
sults from purulent softening of thrombi in the venous sinuses, 
and very rarely it is secondary to leptomeningitis. Not rarely 
localized suppurative pachymeningitis results from disease of the 
middle or internal ear, with extension through the petrous bone. 
The dura becomes thickened by cellular infiltration, is soft and 
edematous, and not rarely undergoes necrotic change. The dis- 
ease may be localized or diffuse, and may occasion secondary 
thickening and adhesions of the dura in cases terminating favor- 
ably. 

Productive pachymeningitis may be of fibrous or ossify- 
ing character. The etiology is often obscure. Some cases follow 
hemorrhagic or suppurative pachymeningitis ; in some the process 
seems to be primarily productive. Traumatism may cause pro- 
liferation of fibrous tissue in the dura. This is especially apt to 
occur after fractures of the skull in children, when, as a result of 
its adhesion to the bone, the dura is almost invariably torn. 
Syphilis is probably a cause of importance. The dura, in the 
fibrous variety, is simply thickened and more or less attached to 
the pia-arachnoid and the inner surface of the skull. When firm 
attachments with the skull are formed, osteophytes are frequently 
found upon the surface of the bones and in the dura (ossifying 
pachymeningitis). Osseous plates may be met with in the falx 
cerebri and tentorium cerebelli. 

INFECTIOUS DISEASES. 

Tuberculosis may occur in the form of miliary tubercles in 
association with tuberculous leptomeningitis. It may also be 
associated with tuberculosis of the bones ; and, in rare instances, 
has been met with as a primary disease of the dura. In the latter 
cases the disease takes the form of a caseous nodular thickening 
of the membrane. 

Syphilis may occasion a form of diffuse productive pachy- 
meningitis, or gummata. The latter may originate in the dura, 
and extend to the pia or skull-bones, or they may originate in the 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 733 



bones and invade the dura secondarily. Gummata in this situa- 
tion present themselves as more or less flattened nodular growths 
of grayish color, having a marked tendency to caseous change 
and to resolution, with formation of circumscribed thickenings 
and adhesions of the dura. 

TUMORS. 

Tumors of the dura mater occur with considerable fre- 
quency. The most common is probably alveolar sarcoma. This 
may occur in various situations, either as a flat swelling, or as a 
somewhat pyramidal mass, with the apex toward the brain, into the 
substance of which it projects ; it is often firmly attached to the skull. 
Other forms of sarcoma are angiosarcoma, characterized by the pro- 
liferation of the cells of the adventitia of the blood-vessels, and a 
form in which the fibrous tissue so predominates as to make it really 
& fibroma, although nests of endothelial cells are found scattered 
throughout it. Other forms of sarcoma, however, also occur, par- 
ticularly a small round-cell variety, which is usually multiple and 
the result of metastasis from some other portion. The latter 
tumors are usually flat, diffuse, and often extensive. They may 
or may not cause bulging of the skull. 

Recent investigations have shown that endotheliomata are 
among the most common tumors in this region. They usually 
occur as single irregular masses ; but occasionally they are mul- 
tiple, and it is possible that under these circumstances metastasis 
has occurred. Ordinarily they produce no disturbances in the 
brain, but in a few instances pressure-symptoms have been re- 
ported. In any of these forms, but particularly in those in 
which the fibrous connective tissue is in excess, calcareous 
infiltration is not uncommon. In nearly all cases these 
tumors may produce erosion of the inner surface of the 
skull. Hyaline degeneration of the intercellular substance is 
very common. Among the other tumor-like growths are fibrous 
changes that may or may not be inflammatory in nature, and lead 
to circumscribed or diffuse thickening of the dura mater, and 
usually cause it to adhere densely to the skull. These are most 
apt to be found in old people. In addition to the round-cell sar- 
coma, gliosarcoma of the brain and carcinoma of the scalp may 
give rise to secondary growths in the dura mater, but these are 
extremely rare. 

CYSTS. 

Cysts of the dura are usually due to its protrusion 
through the skull, and the escape into the protruded portions 
of cerebrospinal fluid. This is spoken of as meningocele. Two 
varieties are recognized, true and false. True meningocele is pro- 



734 



TEXT-BOOK OF PATHOLOGY. 



duced by the bulging of the dura mater through some congenital 
fissure in the skull. It is difficult to distinguish this from 
encephalocele (q. v.). False or spurious meningocele is almost 
invariably the result of some injury before the third year of life. 
There is fracture of the skull and effusion of blood. Later the 
blood is absorbed and replaced by a clear fluid, leaving only a 
brownish layer upon the inner surface of the cyst. As in early 
life the dura is adherent to the skull, it is usually torn at the time 
of fracture ; and ordinarily there is also a laceration of the 
arachnoid, allowing the escape of the cerebrospinal fluid into the 
sac, which is formed externally chiefly by the pericranium. As a 
result of pressure, of bone- absorption, or of defective growth, the 
opening in the skull usually enlarges considerably, and ultimately 
there is extreme deformity of the head. In cases where the brain 
has been lacerated at the time of injury, porencephalic cavities 
may occur, which in some instances have communicated with the 
lateral ventricles. The commonest situation for these cysts is the 
parietal bone ; but they may occur in the frontal or occipital 
regions, and in rare cases are multiple. 

THE PIA AND ARACHNOID. 

CIRCULATORY DISTURBANCES. 

Anemia of the pia may occur in cases of general anemia. 

Active hyperemia is constantly present in the early stages 
of meningitis. It is also met with in cases of death from alcohol- 
ism, and in severe infectious fevers, though in most of these cases 
microscopic examination discloses the fact that the process is really 
one of beginning inflammation. The pia is red and the small 
arterioles are injected. The fluid in the subarachnoid space is in 
excess, and may be slightly turbid or sanguinolent. 

Passive hyperemia occurs in cases of general venous stasis, 
as in heart-disease, pulmonary disease, and venous thrombosis. 
The large veins are greatly swollen, and the subarachnoid fluid is 
excessive. 

Hemorrhages. — Small punctate hemorrhages may occur in 
cases of meningitis, in scurvy, purpura, and the like. Larger 
hemorrhages between the pia and arachnoid are most commonly 
due to traumatism, and may sometimes be the result of rupture of 
aneurysms. The blood in cases of large hemorrhages may cause 
injurious cerebral compression, if death does not follow the injury 
itself. Occasionally the blood becomes inspissated and absorbed, 
the membranes in these instances becoming thickened and pig- 
mented, or it may be encapsulated and the pigment absorbed, 
giving rise to a clear cyst (hygroma). 

I£dema of the membranes, or collections of liquid in the sub- 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 



735 



arachnoid space (external hydrocephalus), may be due to passive 
congestion. The membranes are thickened and of a translucent 
or gelatinous appearance ; the subarachnoid fluid causes elevation 
of the arachnoid and more or less compression of the cere- 
bral convolutions. Hydrops ex vacuo is a form of dropsical effu- 
sion under the arachnoid, resulting from atrophy or hypoplasia of 
the cerebral convolutions. The space normally occupied by cere- 
bral substance is in these cases filled with cerebrospinal liquid. 

INFLAMMATION. 

Inflammation of the arachnoid and pia is called lepto- 
meningitis. It is always an infectious process, and may be 
either acute or chronic. 

Etiology. — The commonest cause of acute leptomeningitis is the 
pneumococcus. It is found in about 60 per cent, of all cases, and 
in these pneumonia is often an associated or primary condition. 
The pneumococcus may reach the meninges either by the blood- or 
lymph-channels, or by creeping along the lymphatic spaces in the 
areolar tissue between the esophagus and vertebral column ; occa- 
sionally it enters directly from the ear or nasal cavity. Other 
micro-organisms that have been found are the streptococcus, the 
staphylococcus, Friedlander's bacillus, the Bacillus pyocyaneus, 
the bacillus of glanders ; the actinomyces, the typhoid bacillus 
(of which a number of cases have been reported), the Bacillus 
coli communis, and the bacillus of bubonic plague. Meningitis 
occasionally occurs in the course of gonorrhea, but no case has as 
yet been reported in which the gonococcus was certainly demon- 
strated. Mixed infection is not uncommon, consisting usually of 
the pneumococcus and one or other of the more common pyogenic 
micro-organisms, and the latter are also frequently found associated 
with the tubercle-bacillus. The cause of epidemic cerebrospinal 
meningitis is the Diplocoeeus intracellular is meningitidis, discov- 
ered in 1887 by Weichselbaum in six cases that he examined, and 
subsequently found in other cases by Goldschmidt, Guarnieri, 
Netter, Faber, and others. 

Pathologic Anatomy. — The gross changes may vary from those 
that are not recognizable macroscopically, to collections of green- 
ish pus in the subarachnoidal space half an inch or more in thick- 
ness and covering the entire surface of the brain. In the slight- 
est forms the presence of the condition may be suspected by the 
slight edema of the arachnoid, and perhaps a small collection of 
fluid containing flakes along the fissures of the brain. In some 
cases, however, even this does not occur, and it is impossible, with- 
out a microscopic examination, to say that inflammatory processes 
exist. Microscopically, sections in these cases usually show over- 
filling of the small vessels with blood, and a greater or less num- 



736 



TEXT-BOOK OF PATHOLOGY. 



ber of round cells, usually polynuclear, immediately surrounding 
it. Often this collection of round cells is most marked in the 
recesses of the convolutions. Staining for bacteria usually reveals 
the presence of a few, although in these cases they are rarely nu- 
merous. If the process has been more severe, or of longer dura- 
tion, the edema of the arachnoid becomes more pronounced ; its 
glassy, moist appearance being very distinctive. The vessels are 
usually injected; and this applies particularly to the veins, which 
appear as dark-blue tortuous cords running through the mem- 
branes. In the subarachnoidal space there is now a considerable 
collection of fluid, aud along the sides of the arteries usually a 
distinct collection of lymph or pus. Sometimes, but not always, 
the arterioles are also distinctly injected, and occasionally there is 
a faint pinkish coloration, due to the injection of the capillaries. 

This form may be localized or diffuse, and is usually secondary 
to some local source of inflammation, which is most frequently 
middle-ear disease. The process often shows distinct indications 
of rapid extension. 

The diffuse forms have been divided (according to the part 
affected Avith greatest intensity) into leptomeningitis of the vertex 
and leptomeningitis of the base. Ordinarily the purulent exudate 
is most pronounced along the course of the middle cerebral artery, 
extending from either side of the sella turcica outward and upward* 

The changes observed consist of diffuse injection of the soft 
membranes, edema of the arachnoid, and a perivascular sero- 
fibrinous exudate along the course of the vessels coming from the 
veins. Microscopically, sections show around these vessels a mass 
of fibrin, in which are embedded a considerable number of poly- 
nuclear leukocytes. Often cells undergoing fatty degeneration are 
also found in these masses, lying close to the walls of the vessels 
in the portions of the brain where the changes are most pro- 
nounced. In this condition micro-organisms are usually found 
quite readily, either within or without the cells, those within the 
cells, in particular, frequently showing a partial loss of staining- 
power, that has been taken to indicate phagocytic activity. 

In the most severe cases the entire subarachnoidal space is dis- 
tended with a purulent accumulation. The surface of the brain 
can no longer be seen, the thick greenish exudate covering the 
convolutions as a smooth mantle. In nearly all these cases there 
is also pronounced edema, the arachnoid looking thick, shiny, and 
moist. Microscopic sections show the ordinary picture of a puru- 
lent accumulation ; pus-cells in a fibrinous meshwork, desquamated 
endothelial cells, and micro-organisms. In all forms of acute 
leptomeningitis petechial hemorrhages into the arachnoid are com- 
mon. The substance of the brain and cord may also be involved, 
and this involvement may vary from a slight increase of the neu- 
roglia-elements just beneath the pia, to the presence of foci of 



DISEASES OE THE BRAIN AND ITS MEMBRANES. 737 



round cells. These foci are usually found about the small vessels 
or lymphatics dipping in from the pia, the latter situation being 
by far the more frequent. Ordinarily they are microscopic and 
surrounded by a narrow zone of partially degenerated nervous 
substance, outside of which there is again a slight increase in the 
neuroglia-tissue and cells. Occasionally, however, the cerebral 
involvement may be more extensive, and large abscesses are 
formed, leading to the destruction of considerable portions of the 
nervous substance. The nerve-fibers, even those in the neighbor- 
hood of the lesion, rarely show distinct alterations. The ganglion- 
cells, however, exhibit slight diffuseness in taking the stain, or 
irregularities in the arrangement of the chromophilic bodies. If 
the abscesses are larger, either involving or close to the gray sub- 
stance, the ganglion-cells may show extensive degeneration, with 
entire loss of staining-power and fragmentation of the protoplasmic 
processes, nothing being left to indicate the position of the cells 
excepting an irregularly shaped vesicle containing some brownish 
pigment. These larger foci, however, are usually found in the 
white substance. 

An attempt has been made to distinguish varieties of menin- 
gitis according to the infective agents, and ^setter has stated that 
in pneumococcic infection the pus is viscid and greenish ; in strep- 
tococcic infection, more serous and less adherent to the mem- 
branes. Honl believes that only four forms can be differentiated — 
the thick, viscid pus of the pyogenic micro-organisms, the yellow- 
ish exudate of tuberculosis, the bluish-green pus of the Bacillus 
pyocyaneus, and the purulent exudate containing yellowish grains 
of actinomyces. 

Epidemic cerebrospinal meningitis does not differ essen- 
tially from the ordinary septic form, excepting in its cause. 
As a general rule the inflammatory process begins upon the 
convexity of the frontal lobes, and proceeds backward and down- 
ward, the basal meninges being involved late in the course of the 
disease. Aside from those forms occurring as a complication of 
other pathologic conditions that lead to death before the menin- 
gitis has been fully developed, it is the one most likely to kill the 
patient before distinct alterations have become evident. These 
cases are spoken of as foudroyant or fulminant. The disease is 
often accompanied by lesions in other parts of the body, as pete- 
chias in the skin, suppuration in the joints, multiple abscesses, en- 
docarditis, degenerations of the myocardium, and suppuration of 
the labyrinth of the ear. 

Associated Changes. — Besides the meninges of the brain, those 
of the cord are almost always involved, even in cases of tuber- 
cular meningitis. The peculiarities of these conditions are de- 
scribed in the section on the spinal cord. Extension along the 
fold of pia mater that covers the choroid plexus is also exceed- 

47 



738 



TEXT-BOOK OF PATHOLOGY. 



ingly common. The cerebrospinal fluid may be turbid, there is a 
moderate amount of lymph on the ependyma and over the surface 
of the plexus, and the latter may even contain small abscesses. 
Not infrequently, in prolonged cases, meningitic adhesions and 
occlusion of the aqueduct of Sylvius give rise to an acute hydro- 
cephalus. 

INFECTIOUS DISEASES. 

Tuberculous meningitis is usually a secondary affection, 
although in children it may occasionally appear in connection with 
a few recent foci in other parts of the body. The bacilli reach the 
meninges ordinarily by the blood-vessels, particularly, in all prob- 
ability, by the left carotid, from which situation they may spread 
along the base or to the vertex. Occasionally they seem to pass 
up the vertebral arteries, and may then affect the cerebellum more 
severely than the base of the cerebrum. Tuberculosis may also 
extend directly from the tubercular lesions of the skull or of the 
middle ear, and it has occasionally been observed to occur after 
traumatism. Other routes of infection, however, have been sug- 
gested, particularly, as in acute purulent meningitis, the organisms 
have been supposed to pass up the posterior mediastinum, the retro- 
pharyngeal areolar tissue, and thence into the cranial cavity. Mixed 
infection not infrequently occurs, and has been supposed to account 
for the purulent exudate. It is certain, however, that pure tuber- 
culous meningitis may occasion the formation of pus. The organ- 
ism that is most frequently found in connection with tubercle- 
bacillus is the pneumococcus, and it may be found intimately 
associated, although it has been stated that the tubercle-bacillus 
appears to predominate at the base of the brain and the pneu- 
mococcus in the exudate of the convexity. 

Pathologic Anatomy. — In cases that die of pulmonary tubercu- 
losis it is not uncommon to find, particularly upon the convexity 
of the pia mater, a number of small grayish nodules. These are 
not always apparent upon superficial inspection, but by cutting 
through the cerebral hemisphere as far as the pia, and then strip- 
ping it away from the under surface of the membrane and holding 
the latter up to the light, they may readily be seen. In certain 
cases tubercle-bacilli have been found when recognizable macro- 
scopic lesions were entirely absent. Microscopic examination, 
however, has usually revealed a few masses of epithelioid cells 
and some slight perivascular round-cell infiltration. 

When the infection is more severe the tubercles are usually 
most numerous upon the base of the brain, particularly on either 
side of the carotid canal and in that part of the base just poste- 
rior to the dorsum sellse. Ordinarily the disease assumes the form 
of disseminated miliary tuberculosis. The tubercles are situated 
between the arachnoid and the pia, often in the depths of the sulci. 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 739 



They vary in size up to 0.5 cm. in diameter, and often show slight 
cheesy degeneration in the center. The meninges are congested, 
and usually there is an exudate of inflammatory liquid that contains 
flocculi of lymph, or is even seropurulent in character. Micro- 
scopic examination shows that the tubercles are composed of epi- 
thelioid cells, which occasionally present some evidence of division. 
Giant-cells are also present, although perhaps not so frequently as 
in lesions in other parts of the body. There is usually round-cell 
infiltration about the vessels, and the latter are apt to be distended. 
This round-cell infiltration may also extend into the cortex of the 
brain, and the tubercles are often found in the latter situation. 
Tubercles may also exist in the choroid plexus. Sometimes, if the 
process has lasted for some time, and the tubercular masses have in- 
creased in size, they may undergo cheesy degeneration and form ir- 
regular masses ; these are usually found at the base of the brain, and 
often cause serious pressure upon the cranial nerves that they involve. 

Occasionally, when only a small number of bacilli have reached 
the meninges and have been deposited in one point, a single cheesy 
nodule may be found, particularly in one of the sulci, forming the 
meningeal tyroma, that sometimes attains a considerable size. In 
these less acute cases the exudate is considerable, and involves not 
only the subarachnoidal space, but also the ventricles of the brain, 
causing a condition that was formerly described as acute hydro- 
cephalus. Numerous tubercles are found in the choroid plexus, 
and the ependyma is covered with slight elevations resembling 
somewhat the appearance of cor villosum. These are usually 
found to consist of proliferated endothelial cells and of the sub- 
ependymal neuroglia and fibrous tissue. Tuberculous infiltration 
of the brain-substance is, however, very common. This may 
be either nothing more than an extension by continuity along the 
lymph-spaces and blood-vessels dipping from the pia or ependyma 
into the brain-substance, and giving rise to small foci composed of 
epithelioid and giant-cells surrounded by leukocytes, and perhaps 
exhibiting a slight degree of cheesy degeneration in the center ; or 
else considerable areas of softening, which are perhaps caused by 
the formation of thrombi. These are most frequent in the corpus 
striatum and the crura, and appear as grayish-white or yellowish 
areas of softened and degenerated nervous tissue. Not infre- 
quently, punctiform hemorrhages are found in the cortex about 
these areas of softening. The tubercle-bacillus is usually readily 
found, although this is practically impossible if the tissue has been 
hardened in Miiller's fluid. In general, extension of the tuber- 
cular process to the meninges of the cord occurs if the duration 
of the process is at all prolonged, but the vertebral canal is so 
much longer than the spinal cord that pressure-symptoms rarely 
occur, and, as the irritation is slight, the cranial symptoms domi- 
nate the clinical course. 



740 



TEXT-BOOK OF PATHOLOGY. 



Syphilis may occur in the form of gummatous infiltration. 
In these instances there are found flattened nodular thickenings 
of the arachnoid and pia, of grayish or pinkish color, and tending 
to undergo necrotic change. The process begins in the inner 
surface of the arachnoid, or sometimes in the walls of the blood- 
vessels, and extends to the pia and cerebral substance on the one 
hand, and to the dura on the other. In another form of syphilis 
there is diffuse infiltration or syphilitic leptomeningitis, causing 
considerable thickening of the meninges. 

Chronic syphilitic leptomeningitis and meningo-encephalitis are 




Fig. 346— Gummatous meningo-encephalitis (Ziegler). 



occasionally met with. In these cases the membranes are thick- 
ened and fibrous, and secondary extension of the infiltration into 
the cerebral cortex occurs (Fig. 346). 

TUMORS. 

The Pacchionian Bodies. — The most common, and clini- 
cally perhaps the least important, tumors of the arachnoid are the 
Pacchionian bodies. These occur as small granular masses or 
circumscribed nodules, chiefly along the upper edge of the superior 
longitudinal sinus, often extending a short distance laterally over 
the convex surface of the convolutions. Microscopically they 
consist of dense masses of fibrous tissue, covered by a layer of 
proliferated endothelial cells, which give them a concentric struct- 
ure. Occasionally some calcareous nodules may be found in them. 
They usually grow only outwardly, and frequently erode the skull, 
giving rise to little pits upon the inner surface. 

I^ndotheliomata are most frequently found in the pia mater. 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 741 



They occur as irregular alveoli, lined with cuboidal or round endo- 
thelial cells. These are not always arranged in a single layer, but 
may occasionally fill the alveolus, although this is not common, and 
more frequently some have broken loose and lie free in the cavity. 
The cells often show karyokinetic changes, and occasionally alter- 
ations in shape, due to mutual pressure. These tumors resemble 
carcinomata closely, but the presence and proliferation of the 




Fig. 347.— Endothelioma of the pia mater. 



epithelium-like cells in the stroma, such as occur in carcinoma, 
have not been observed (Fig. 347). 

Cholesteatomata are of two kinds : those consisting exclu- 
sively of squamous epithelial cells, and those containing, in addition, 
various other epidermal structures, such as hairs or sebaceous 
glands. They are usually situated in or about the median line, 
along the base of the brain or on the upper surface of the corpus 
callosum, or somewhere along the choroid plexuses. Those con- 
taining hair are most frequently found near the cerebellum, grow- 
ing either from the arachnoid, or, more rarely, from the outer sur- 
face of the dura. The latter may occur upon the frontal or occip- 
ital bones, and often show calcareous infiltration, or even true 
osseous formation. 

I/ipOtnata are rare. They are usually found in children, and 
always in the soft membranes, especially the pia mater. The 
most frequent seats are the upper surface of the corpus callosum 
and the corpora candicantia. According to Bostroem, they are 
probably epidermal in origin, nothing but the subcutaneous fatty 
tissue being left. 



742 



TEXT-BOOK OF PATHOLOGY. 



Teratomata may be present. Chiari has described a case 
that grew from the lining membrane of the third ventricle in an 
infant that died at the age of seven weeks. It consisted of a 
medullary white mass and a number of serous cysts. The solid 
substance was composed of fetal brain-substance, in which were 
fissures lined with epithelium similar to that of the central canal 
of the cord, and ganglion-cells, retinal cells, skin-glands, and jelly 
of Wharton. Fibrous and cartilaginous tissues were also present. 

THE BRAIN. 

Physiology. — The functions of the membranes of the brain 
are partly protective, partly nutritive. The dura serves to nour- 
ish the under surface of the skull, to enclose the sinuses carrying 
blood away from the brain, and to protect the brain itself. As a 
result of laceration, it may allow the brain to protrude, and any 
condition obstructing the sinuses naturally gives rise to passive 
congestion. The arachnoid is a delicate membrane intimately 
associated with the pia, from which it is separated by an areolar 
connective tissue in whose meshes the cerebrospinal fluid circu- 
lates. As this is very distensible, in all cases of passive conges- 
tion or edema of the brain a considerable amount of fluid is 
found between these two membranes. It acts thus as a sort of 
safety-valve. The pia forms a delicate fibrous membrane inti- 
mately associated with the surface of the cerebral convolutions. 
Any lesion of it therefore involves the brain-substances. 

DEVELOPMENT AND ANATOMY. 

Development. — (For convenience, the development of the cord is con- 
sidered in this place with that of the brain.) The central nervous system 
commences as a shallow depression, that appears in front of the primitive 
streak in early embryologic existence. It is bounded on either side by ridges, 
known as the medullary folds. The groove gradually becomes deeper, and 
finally the two medullary folds unite, giving rise to the formation of the 
medullary canal, which is soon separated from the dorsal surface of the em- 
bryo by the interposition of mesoblastic tissue. The canal is first formed 
in the portion that subsequently forms the cervical region of the spinal cord. 
Just beneath the medullary canal there is a cylindrical collection of cells, 
often with a small cavity in the center that forms anteriorly a shallow groove, 
the so-called notochord. Its function is unknown, and it eventually disap- 
pears during embryonic existence, although traces may still be found in the 
intervertebral cartilages at birth. In some of the lower animals a small 
sac-like dilatation is found anteriorly, from which a process extends down- 
ward and apparently stops at the hypophysis cerebri ; but it is not certain 
that it forms a portion of this organ. The anterior extremity of the embryo 
continues to grow, and bends downward, forming the cephalic fold. In 
this part of the neural canal three dilatations occur — the primary vesicles 
of the brain; the posterior portion ultimately forms the spinal cord. 

The Cord. — At first the wall of the embryonal cord is composed of a 
single layer of cylindrical epithelial cells {spongioblasts), with nuclei at 
various distances from the central canal; these ultimately become the 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 743 



nuclei of the glia-cells. The central ends remain cylindrical ; the periph- 
eral ends become branched, forming the myelospongium, probably the 
antecedent of the neuroglia-fibers, which, according to some recent investi- 
gations, become separated from the cells. At the age of about five weeks 
in the human embryo, certain cells, with a considerable amount of clear 
protoplasm, are found near the inner limiting membrane, the so-called 
germinal cells. Subsequently other cells appear, probably derived from the 
germinal cells, as they are first found in the situations occupied by these, 
the so-called neuroblasts. These are distinguished by the appearance of a 
projection, pointing toward the periphery of the spinal cord, that grows 
out from the protoplasm and ultimately pierces the external limiting 
membrane to become an axis-cylinder. The central canal, at this period, 
is usually elliptical in shape, with the long axis dorsoventral. The anterior 
and posterior ends are very thin, and the former ultimately becomes invagi- 
nated to form the anterior commissure. 

Just outside of the cord, probably from masses of epiblastic cells derived 
from its wall, the cells of the spinal ganglia appear. These are, at first, 
bipolar, one process extending into the spinal cord, and the other peripher- 
ally, but ultimately the two processes unite at their commencement. The 
spinal cord at first completely fills the spinal canal, but after the fourth 
month the vertebral column begins to grow somewhat more rapidly, and 
at birth the conus terminalis is opposite the third, and in the adult extends 
only to the lower end of the first, lumbar vertebra. The nerve-fibers are 
at first non-medullated, but later myelin-sheaths appear, first in certain 
parts of the posterior columns, and lastly in the pyramidal tracts, which 
often, at birth, are not yet entirely medullated. The membranes are 
derived from the mesoblast. 

The Brain. — The three primary vesicles from which the brain is devel- 
oped continue t© grow, and the first is subdivided by a median constriction 
into two secondary vesicles, the prosencephalon and the thalamencephalon. 
From the former two lateral offshoots appear, which give rise to the 
cavities of the lateral ventricle ; and from the walls of these are developed 
the cerebral hemispheres, the olfactory lobes, and the corpus callosum. 
The cavity of the second vesicle forms the third ventricle, and from its w r alls 
grow the nervous part of the eye, the optic thalami. and the pituitary 
and pineal bodies. The cavity of this vesicle (mesencephalon) forms the 
aqueduct of Sylvius, and from its walls grow the corpora quadrigemina 
and the crura. The posterior primary vesicle also becomes constricted, 
forming the epencephalon and the metencephalon. The two cavities, 
however, remain united and form the fourth ventricle. From the walls 
of the anterior portion are developed the cerebellum and the pons. From 
those of the posterior portion, the medulla oblongata. 

The ultimate shape of the brain, however, is largely determined by certain 
flexures and by the growth and extension of the axis-cylinders, which pass in 
various directions and form the white matter, the greater bulk of the central 
nervous system. The first flexure is beneath the mesencephalon and concave 
■from the ventral surface. The second flexure is concave dorsally, and is just 
beneath the epencephalon. The third grows at the junction of the meten- 
cephalon with the spinal cord, and is concave ventrally. Differing from 
the cord, the growth of the brain exceeds that of its containing bony cap- 
sule. As a result the surface of the hemispheres is usually thrown into 
folds. The earliest of these appear during the third month, and are usually 
transverse to the axis of the brain, although not invariably. The lateral 
ventricles at this stage are very large, and the sulci project into their cavi- 
ties as ridges. During the fourth month they disappear, with the exception 
of three — the Sylvian, the calcarine, and the parieto-occipital fissures. The 
hippocampal fissure also appears about this time. The other permanent 
sulci appear about the end of the fifth month, the earliest being the fissure 



744 



TEXT-BOOK OF PATHOLOGY. 



of Rolando ; but many of the secondary fissures do not develop until after 
birth. 

The sympathetic nervous system is probably only an offshoot of the 
central nervous system. The cells first appear upon the spinal nerves, from 
which they wander, remaining connected with them by short branches, 
the rami communicantes. Some authorities, however, believe that the 
sympathetic system is developed from the mesoblast. 

Anatomy. — The brain consists of the two cerebral hemispheres, the 
basal ganglia, the pons, the medulla, and the cerebellum. Its weight varies 
from 1200 to 1300 grams in the adult female, and from 1300 to 1400 grams 
in the adult male. Its consistency at birth is very soft; in the adult it 
becomes somewhat firmer, but is always softer than the normal liver. Its 
color varies from grayish-white in the parts composed of medullated fibers, 
to reddish-gray in those composed chiefly of ganglion-cells. The cerebral 
hemispheres are two large symmetrical masses occupying the greater por- 
tion of the cranial cavity; they are separated by the superior longitudinal 
fissure, and united by the corpus callosum and the anterior commissure. 
They are joined to the pons by the crura. Their surfaces are rendered very 
irregular by the presence of numerous fissures or sulci; and are divided into 
the frontal, parietal, occipital, and temporosphenoidal regions. The impor- 
tant fissures are the Sylvian, the Eolandic, and the parieto-occipital on the 
external surface ; the calloso-marginal, the calcarine, and the parieto- 
occipital on the medium surface. 

The hemispheres are composed essentially of an outer layer of gray 
matter, the cortex, containing ganglion-cells, and of fibers passing from 
these in various directions and uniting them with other parts of the central 
nervous system. These may be divided into three main classes : the pro- 
jection-fibers, passing between the cortex and the basal ganglia, or into the 
internal capsule ; the transverse or commissural fibers, passing between two 
hemispheres ; and the association-fibers, passing between different areas in the 
same hemisphere. The most important clinically of the projection-fibers are 
those which arise in the motor portion of the cortex, and pass first into 
the internal capsule, where they are grouped about the knee, thence through 
the crusta and the pons, to form ultimately the pyramids of the medulla. 
They decussate in the first cervical segment of the cord and form the pyram- 
idal columns of the cord. The fibers of the optic radiation commence 
in the cortex about the calcarine fissure and in the cuneate lobe, and pass 
forward to the pulvinar of the optic thalami. They are also associated 
with the external geniculate body and the anterior corpus quadrigeminus. 
From the pulvinar, the optic tracts pass around the crusta, then lie below 
and to the inner side of the internal capsules, and unite in front of the 
tuber cinereum to form the chiasm from which the optic nerves arise. 
The transverse or commissure-fibers include those of the corpus callosum 
and of the anterior commissure. The fibers in the corpus callosum appear 
to correspond closely to those regions of the brain situated nearest to them. 
The anterior commissure is composed of fibers uniting the temporosphe- 
noidal lobes of the two hemispheres. The association-fibers either connect 
adjacent lobes {fibrce proprice), or unite distant portions of the hemispheres 
(the long association-fibers). The most important of the latter are the 
superior, interior, and anterior association-bundles, the cingulum, and the 
fornix ; the latter is a group of arching fibers connecting the hippocampal 
region with the corpora albicantia. 

In the substance of each hemisphere are found the lateral ventri- 
cles : two long, narrow, branching cavities, joined to the third ventricle 
by the foramen of Monro. Each contains a choroid plexus, and is nor- 
mally lined with epithelium and contains clear cerebrospinal fluid. The 
anterior portion of the two ventricles is separated by the septum. A small 
double layer of epithelial cells line and almost fill the cavity of the fifth 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 745 



ventricle. The basal ganglia of the brain are the lenticular nucleus, the 
caudate nucleus, forming together the corpus striatum, and lying on either 
side outside of the internal capsules, the optic thalamus, a large oval mass 
lying beneath the caudate nucleus. The outer portion on the lenticular 
nucleus is usually known as the putamen ; the two inner segments are 
known together as the globus pallidus. To the outer side of the 
putamen is a band of white fibers, known as the external capsule, that 
is separated from the cortex by a thin layer of pigmented cells, the 
claustrum. 

The third ventricle communicates with the fourth by a narrow canal, 
the aqueduct of Sylvius, which passes through the tegmentum of the crura. 
It is surrounded by a zone of gray matter, in which are found the nuclei of 
the oculomotor nerves. Above it are the four corpora quadrigemina ; two 
pairs of rounded eminences with a white cortex and a gray center. The 
superior corpora, as has been already stated, are intimately connected with 
the optic tract. Just anterior to these bodies is the small pineal gland, a 
hypoplastic median eye situated above the posterior commissure. Exter- 
nally to the crusta on either side, continuous with the posterior portion of 
•the thalamus, are the two geniculate bodies, separated by the optic tract, 
with which the external geniculate body is closely connected. The optic 
thalami lie on either side of the third ventricle, and just beneath the cau- 
date nuclei ; they are oval bodies containing numerous groups of nerve- 
cells, the anterior portion being called the anterior tubercle, and the pos- 
terior portion the pulvinar. 

The two great channels by which fibers pass to and from the cerebrum 
are the crura cerebri. These are divided by a narrow layer of dark -gray 
material, the substantia nigra, composed of pigmented ganglion-cells, into 
the crusta, or inferior portion, and the tegmentum, or superior portion. 
A part of the crusta is formed, as has already been stated, by the pyram- 
idal tract. Sensory nerve-fibers are found in two groups in the tegmen- 
tum toward the outer edge, comprising the inferior and superior fillets. 
These fibers divide into three bands : one passes into the superior portion 
of the tegmentum, and some of these enter the posterior portion of the 
interior capsule; another band passes to the anterior corpora quadrigemina 
and the thalamus ; and a third into the posterior corpora quadrigemina, 
although it is not certain that all the fibers are thus distributed. 

The two crura unite to form the pons, which is composed, ven- 
trally, of bundles of motor fibers separated by the commissural fibers 
of the cerebellum, and dorsally, partly of the fibers of the fillet and partly 
of gray matter. Below the pons is found the medulla, which is really noth- 
ing but the upper portion of the spinal cord. Anteriorly we find the two 
well-defined bundles of motor fibers, the pyramids; just back of these the 
lower olives ; and on the dorsal surface the nuclei of the tenth and twelfth 
nerves, and externally to them the nucleus gracilis and nucleus cuneatus, 
the terminations respectively of the columns of Goll and Burdach in the 
cord. The axis-cylinders of the cells that compose these nuclei pass toward 
the brain and form the fillets. On the outer surface of the medulla, near 
the dorsal surface, are the two restiform bodies, the continuations of the 
cerebellar peduncles. 

The cerebellum is composed of two lobes and the vermiform process. 
Upon cross-section it is seen to be composed of a great number of narrow 
gyri separated by deep ramifying sulci, each convolution being lined 
externally by medullated fibers, beneath which is a layer of ganglion-cells 
enclosing a center of medullated fibers. It is united to the cerebrum by 
the superior peduncles, which terminate in the nucleus ruber of the tegmen- 
tum. The middle peduncles form the transverse fibers in the pons, and 
the inferior peduncles pass into the restiform bodies of the medulla. Certain 
nuclei are found in the interior of the white substance, of which the most 



746 



TEXT-BOOK OF PATHOLOGY. 



important is the dentate nucleus, analogous structurally to the olives of the 
medulla. 

The Neuron. — Histologically the essential element of the nervous sys- 
tem is the neuron. This, in the sense of Waldeyer, comprises the nerve- 
cell, its protoplasmic processes (which are branched), and the axis-cylinder, 
which may be a single fiber giving off lateral collaterals, or is extensively 
branched (Golgi cells). The cell-body consists of protoplasm without a dis- 
tinct cell-wall, and containing or not containing chromophilic bodies. Ac- 
cording to Nissl, two groups of cells are thus formed, the somatochromes 
with, and the caryochromes without, these bodies. According to zoologists, 
these are respectively motor and sensory in function, but the cells of the spinal 
ganglia, which appear to be sensory, contain these granulations. Cells are 
spoken of as multipolar or bipolar, according to the number of processes that 
project from them. It is impossible to describe in this place all the varieties 
of cells and their distribution in the nerve-substance. The neurons may be 
divided into endogenic, wholly within the central nervous system, and 
exogenic, partly in the peripheral nervous system. Each axis-cylinder 
terminates in a tuft of fibers that surround, without touching, some other 
ganglion-cell, or, if it extends to the periphery, terminates in a special sen- 
sory corpuscle or a muscle-plate. 

Physiology of the Brain. — This subject can be touched upon only very 
briefly. The brain is the organ in which all the intellectual processes are 
performed, but it is as yet unknown how this is accomplished. A number 
of theories have been suggested, but none of them are based upon fact. 
We are better informed concerning the origin of certain specific motor im- 
pulses in the brain, and the regions where stimuli from certain of the special 
sense organs are received. The motor region is situated in the two gyri on 
either side of the fissure of Rolando, and in the posterior portions of the 
three frontal gyri. In general, it can be said that the centers are arranged 
so that the cells sending fibers to the highest portion of the body — that is, 
the face, eyes, etc. — are situated in the lowest portion of the motor region ; 
and the cells sending impulses to the lowest portion of the body — the feet r 
for instance — are situated in the highest portion of the motor region along 
the superior longitudinal fissure. This region has been mapped out by the 
aid of direct observation, not only upon the lower animals but upon human 
beings. Any irritation causes movement of the corresponding portion of 
the body, the movement being of a co-ordinated and not of an individual 
muscular type ; that is to say, the stimulation of a center in this region 
causes contraction of a number of muscles, with the object of accomplish- 
ing some definite movement. The fibers of the motor region constitute the 
pyramidal tract, whose course has already been described. Irritative 
lesions of the motor cortex produce convulsive explosions, clonic in type, 
usually described as epileptic. If the lesions are sharply circumscribed,, 
and the convulsions occur always in a certain definite group of muscles, 
the epilepsy is spoken of as Jacksonian. Destructive lesions cause paraly- 
sis of a spastic type ; that is to say, the lower motor neurons evidently suf- 
fice to maintain a condition of contractility in the muscles, which may be 
exalted either as a result of some irritation exerted by the degenerated cen- 
tral motor neurons, or because, under normal conditions, the central motor 
neurons exert an inhibitory or restraining action. We are still in ignor- 
ance concerning the localization of the sensory impulses. The effect of 
lesions in the upper portion of the parietal lobe in producing sensory forms 
of muscular inco-ordination has led to the supposition that the fibers con- 
veying muscular sense terminate in this region. It is practically certain 
that the great majority of the sensory fibers terminate in the optic thala- 
mus, from which other fibers proceed to the cortex ; but as brain physiol- 
ogists are practically agreed that all the active intellectual processes are 
accomplished in the cortex, it is supposed that the thalamus is merely a 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 747 



situation in which some alteration or modification of the impulses re- 
ceived from the periphery occurs. Regarding the special senses, the visual 
impressions terminate in the cuneus. The auditory centers are situated in 
the superior temporosphenoidal convolutions, and the destruction of these 
centers produces loss of understanding of sounds heard — that is to say, 
sensory aphasia. The centers for olfaction are situated in the uncinate 
gyri. Irritation of these regions has in some cases apparently given rise to 
subjective odors, usually disagreeable. They may occur as the aurae of 
epileptic attacks. The center for gustation has not been located, although 
it is probably in this region. The functions of the remaining portions of 
the cortex are practically unknown. It is supposed that the intellectual 
processes are performed chiefly in the frontal lobes. At any rate, extensive 
lesions of these lobes have caused alterations in character — loss of the 
faculty of attention, more or less stupidity, and hebetude. Occasionally 
ataxia is present. The relation of pathologic processes in the brain to 
insanity is not well determined. Lesions have, of course, been found in 
paretic dementia, in acute delirium, and in idiocy, but examination of the 
brain in cases of paranoia and melancholia has been practically negative. 
The functions of the other portions of the brain are not well determined. 
The basal ganglia are apparently merely stations in the paths of the fibers, 
chiefly those of sensory nature. The anterior corpora quadrigemina have 
something to do with the fibers of the optic tract, and in them is probably 
, situated the center of the pupillary reflex to light. The external genicu- 
late ganglia are apparently associated with the fibers conveying auditory 
impressions. The pons contains the ganglion-cells of the peripheral motor 
neurons of the eye-muscles, but is otherwise merely a pathway for various 
tracts of fibers. The medulla contains the ganglion-cells of the cranial 
nerves, and, in addition, all the tracts of fibers passing between the brain 
and cord. The functions of the cerebellum are not well known. There is 
no doubt that it has something to do with equilibration, but the lesions 
must be situated either in the vermis or bilaterally. 

Preservation of the Brain and Cord. — After the brain has been 
removed from the cranial cavity it is probably best to place it at 
once in a 10 per cent, solution of formalin. The formalin should be 
changed at intervals of three or four days. If it is hardened in Mliller's 
fluid, deep incisions should be made, preferably parallel to the upper sur- 
face of the corpus callosum, after the removal of the frontal and occip- 
ital lobes. The fluid should be changed at the end of the first hour, then 
at the end of twelve hours, and then every day for one or two weeks. If it 
is desired to examine the brain at once, it may still be preserved for micro- 
scopic investigation by making two horizontal incisions through the cere- 
bral hemispheres, parallel to the upper surface of the corpus callosum, then 
cutting into the lateral ventricles. If a hemorrhage exist, it can usually be 
detected by the presence of blood in one of the ventricles, or by discolora- 
tions of the floor. The most important part of the brain, for the purpose of 
tracing secondary degeneration, consists of the stem, so called — that is, the 
basal ganglia, the crura, the pons, and medulla. It is usual to make serial 
sections through this part, which may be removed by cutting off the frontal 
lobes at the knee and the occipital lobes opposite the splenium, and then 
removing the temporal portion of the brain by sagittal section just outside 
of the lateral ventricles. As soon as the cord has been removed the dura 
mater should be cut on both sides and laid back. It is usually desirable to 
remove the cord first, as by this means a horizontal section can be made 
through one of the upper cervical segments, and the remainder of the cord 
then removed with the brain. In this manner the usual oblique incision, 
that renders the upper portion useless for microscopic study, is avoided. It 
is unnecessary, and for many reasons undesirable, to make transverse incis- 
ions through the cord before hardening, even if Mliller's fluid be employed. 



748 



TEXT-BOOK OF PATHOLOGY. 



CONGENITAL ABNORMALITIES. 

The deformities of the brain are numerous and complicated. 
They may be divided roughly into those associated with altera- 
tions in the skull and those occurring within the cranial cavity. 

Acrania is a deformity characterized by absence of the skull. 
The membranes are usually preserved, and form a sac filled with 
serum, on the inner surface of which small particles of nervous 
tissue may occasionally be found. More frequently the brain forms 
only a small mass at the upper portion of the spinal canal, lying on 
the basilar process of the occipital bone. Sometimes it appears as 
if the sac had ruptured, or had never completely closed, for the 
membranes are collapsed, and form upon the base of the skull 
a mass consisting of fibrous connective tissue and blood-vessels. 
Often in this case the encephalon is entirely absent, but the pons 
and medulla may be almost completely developed. The cranial 
nerves are present. 

Hemicrania is a condition in which more or less of one of 
the parietal bones, or of a portion of the frontal or temporal bone, 
has failed to develop. The corresponding portions upon the oppo- 
site side that have developed are usually hypoplastic. Ordinarily, 
anencephaly, or else partial development of the brain, is associated 
with these changes. 

Cranioschisis is the name applied to imperfect closure of the 
skull along the middle line. This may be associated with rha- 
ehisehisis, in which case both skull and spine are cleft. The com- 
monest situations for small fissures are in the frontal bone, in the 
region of the posterior fontanelle, in the median line of the pos- 
terior portion of the occipital bone, and, more rarely, in the region of 
the anterior fontanelle or the sagittal suture, or in the sphenoid bone. 

Fissures or other small defects usually occasion hernia of the 
brain, which is named encephalocele, and according to its situation 
anterior or posterior, frontal or occipital, superior, inferior, or 
lateral. If, instead of brain-substance, only the membranes pro- 
trude through the fissure, the condition is known as meningocele. 
In these cases the cavity is filled with cerebrospinal fluid. Some- 
times the under surface of the membrane is lined with nervous 
tissue, showing that it represents a dilatation of one of the pri- 
mary cavities of the brain, corresponding to the condition found in 
spina bifida. These congenital hernise are probably the result of 
fetal hydrocephalus, although it is possible that the chief cause is 
the imperfect development of the cranium. In cases in which the 
fissure is in the sphenoid bone, it is not uncommon to find, as an 
associated condition, cleft palate. Life is, of course, incompatible 
with extensive encephalocele. If it is small, the neck of the sac 
is sometimes constricted, either spontaneously or as a result of 
surgical interference, and recovery ensues. 



DISEASES OF THE BE A IN AND ITS MEMBRANES. 749 



Cyclencephaly is a peculiar deformity in which there is fail- 
ure of the anterior cerebral vesicle to develop. The frontal lobes 
remain fused, and a rudimentary eye develops. 

Abnormalities in Sise. — The size of the brain is subject to 
considerable variation. 

Macrocephaly is the condition in which the brain is excessively 
large — that is, more than 1500 gm. This may be of two kinds. 
In the first, and perhaps less common, form the brain is entirely 
normal in structure, the proportion between the various parts being 
maintained and the relation between the nervous tissue and the 
neuroglia not altered. In some instances the subjects possess un- 
usual intelligence ; in others this is not the case. The second 
form is enlargement of the brain with hyperplasia of the neurog- 
liar tissue. This is not infrequently found in the so-called hyper- 
trophic nodular gliosis. In this condition the brain may be con- 
siderably enlarged, and the convolutions may be increased in size, 
although not abnormal in arrangement. Microscopically, the 
changes described in the section on sclerosis are discovered. A 
pseudo-enlargement of the brain is produced by hydrocephalus. 
The weight of the brain, after the liquid has been removed from 
the cavities, is usually less than normal, although this is not 
always the case. 

Hypertrophy of the brain may be limited to certain parts. 
These are usually individual gyri, and are nearly always sclerotic. 
Sometimes only a portion of a convolution is thus affected, and 
produces a tumor-like swelling. Hypertrophy of individual 
sections of the encephalon does not appear to have been observed ; 
that is to say, simple enlargement of the cerebellum, or of one of 
the cerebral hemispheres. 

Microcephaly is a condition in which the brain is much smaller 
than normal, as a result of defective growth, or else of disease, 
either in early life or later. In some instances the brains, aside 
from their smallness, appear perfectly normal, and this diminution 
in size, within certain limits, is not incompatible with normal in- 
telligence. Usually, however, there are sclerosis and decrease in 
size of some of the gyri. There are, of course, the associated 
changes usually found in sclerotic conditions. 

Hypoplasia of individual portions of the brain has been observed, 
particularly of the corpus callosum, the cerebral hemispheres, and 
the cerebellum. 

Hypoplasia of the cerebral hemispheres is usually due to some 
pathologic change, and will be discussed under sclerosis and poren- 
cephaly. 

The congenital absence, either total or partial, of the corpus 
callosum has been observed in a number of cases. It may occur 
in brains otherwise normal, but is usually associated with micro- 
cephaly or other profound structural changes. In the cases in 



750 



TEXT-BOOK OF PATHOLOGY. 



which no other lesions exist the intelligence may be normal, but 
in the great majority of instances the patients are idiots. In all 
cases, however, the following associated alterations have been 
observed : absence of the calloso-marginal sulcus, division of the 
gyrus fornicatus by perpendicular fissures, the splitting of the 
fornix, and, in certain cases, secondary degenerations. The tape- 
tum is usually intact. The absence of the transverse fibers in the 
centrum ovale renders the superior longitudinal fasciculus very 
distinct. The appearance of the brain is quite characteristic. As 
soon as it is removed the hemispheres fall widely apart, showing 
the third ventricle covered with a delicate layer of pia mater. 
The inner surfaces of both hemispheres are divided by numerous 
fissures, and appear atypical. When only a portion of the corpus 
callosum is absent the splenium is nearly always preserved. In 
cases of marked hydrocephalus the corpus callosum is extremely 
thin, and may be torn during the removal of the brain, and this 
may possibly be mistaken for congenital absence. A careful exam- 
ination, however, will usually reveal the true state of affairs. 

Hypoplasia of the cerebellum, or even total absence of one or both 
hemispheres, has been occasionally observed. It is nearly always 
associated with sclerosis. A collection of cerebrospinal fluid in part 
supplies the place of the absent organ. The cerebellum maybe of 
normal shape, and even microscopically show no changes other than 
diminution in size. More commonly, however, the changes are 
asymmetrical, one lobe being markedly smaller than the other, and 
perhaps reduced even to a small papilla. There are often sclerotic 
changes, with marked atrophy of the cortex and disappearance of 
many of the medullated fibers. In these cases the cerebellum is 
usually of somewhat firmer consistency. The associated changes 
are diminution in size of the olivary bodies ; in the unilateral cases, 
of that upon the opposite side ; the pons and medulla are usually 
smaller than normal, and in the former the pyramidal tracts, on 
account of the absence of the transverse fibers, are usually com- 
pact and distinct. Sometimes the corpora quadrigemina are also 
altered, but this is* not invariably the case. 

Other changes of unknown significance that have been described 
are abnormal arrangement of the convolutions. Of these the most 
important is the presence of annedant gyri across the Rolandic 
fissure, or the absence of annectant gyri in the parietooccipital 
fissure. It does not appear, however, although the claim has been 
frequently made, that these changes are in any way associated 
with intellectual peculiarities. Bundles of nerve-fibers, taking an 
abnormal course, have occasionally been found in the pons and 
medulla. These seem to be produced by premature decussation 
of portions of the pyramidal tract, and are of no clinical sig- 
nificance. 

Anencephaly, or total absence of brain, is a congenital lesion 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 



751 



usually associated with acrania. Sometimes it is associated with 
total absence of the spinal cord ; in other cases a portion of the 
pons, medulla, and the cord are still present, although much 
smaller than normal. The cranial nerves are usually present, and 
the eyes, in particular, are nearly always perfectly developed. 
The lesion is, of course, incompatible with life, although when 
the medulla is present a few respirations may take place after 
birth. The appearance of the monsters is very characteristic. 
From the orbital ridge of the frontal bone the skull slopes in 
almost a direct line to the neck, making the face and eyes un- 
usually prominent — the so-called frog-face. Frequently other 
deformities are also present. 

POST=MORTEM DEGENERATIVE CONDITIONS. 

It is important to be acquainted with the post-mortem altera- 
tions that may take place in the nervous system, in order to avoid 
the confusion of such changes with those that have occurred as 
the result of disease. Little attention has been paid to the macro- 
scopic changes, and they are not characteristic. Their degree 
depends upon the temperature at which the body has been kept 
after death, the nature of the disease that preceded death, and the 
period that elapsed before the tissues are removed. Ordinarily no 
changes will be noticed under thirty-six hours if the body is 
kept on ice. If kept at a temperature of about 16° C. (61° F.), 
the brain and cord will appear normal if removed within twenty- 
four hours. There is first softening of the nervous tissue, that is 
general and not associated with pigmentation ; the tissues may 
become so soft that it is almost impossible to remove them with- 
out injury. Later there is often a considerable extravasation of 
blood-pigment around the vessels ; and, finally, if putrefaction is 
advanced, the tissues become almost diffluent and light brown in 
color. 1 

Lately, Italian authors have studied methodically the micro- 
scopic changes. The nerve-cells swell, their protoplasmic processes 
break off, and there is a gradual loss of the staining-power of the 
chromatin-bodies ; vacuoles appear in the protoplasm and the out- 
line of the cell becomes irregular ; and finally the chromatin- sub- 
stance completely disappears. The outlines of the nucleus become 
indistinct, it swells, and then contracts, with irregularity of the 
outline. It stains homogeneously, due to diffusion of the chro- 
matin, and may contain small granules of hyaline material. It 
is often placed excentrically in the cells. Later it loses its stain- 
ing-power, and finally disappears completely. The nucleolus is 
the last structure to show alteration ; it may swell slightly, be- 
come filled with vacuoles, and then break up into granular mate- 
rial and disappear. The protoplasmic processes do hot exhibit 



752 



TEXT-BOOK OF PATHOLOGY. 



varicosities, but apparently become more fragile, and are very apt 
to be broken off during staining. Changes may take place in the 
myelin-sheaths that, when studied by Marchi's method, are not 
greatly different from those seen in areas of softening — that is, 
small fatty granules appear along the course of the nerve-fiber. 
In post-mortem lesions, however, there is no perivascular round- 
cell infiltration ; no compound granular cells can be found in the 
tissue ; there are no signs of proliferation in the neuroglia ; and 
the process is more general and uniform than is apt to be the 
case in morbid conditions. 

GENERAL PATHOLOGIC ANATOMY OF THE NERVOUS 
SYSTEM. 

The pathology of the nervous system differs from that of the 
other organs of the body chiefly in the fact that the special struct- 
ures of which the nervous tissue is composed have no close anal- 
ogies to the epithelial cells and connective tissues. It is desirable, 
therefore, to discuss, first, the general changes occurring in the 
nerve-cells, nerve-fibers, and the neuroglia. 

The Nerve=cell. 

Of late years, considerable progress has been made in the 
elucidation of the finer pathologic changes that occur in the nerve- 
cell. On account of their characteristic appearance and sharply 
differentiated structure, the cells of the anterior cornua of the 
spinal cord have been most carefully studied, and it is necessary, 
therefore, that we should give a brief description of their anatomy. 
The appearance depends largely upon the method of staining em- 
ployed. By the Golgi method the cell appears as an irregular 
body, from which come a number of thick processes, that rapidly 
divide and subdivide, until they appear as a maze of independent 
delicate branches, upon either side of which can be seen minute 
projections, the so-called gemmules ; from one portion of this cell 
a fine process arises that is of uniform width, the neuraxon. At 
regular intervals this gives off the so-called collaterals, delicate 
branches that spring from it at right angles and have a differ- 
ent course. By this method other ganglion-cells in the nervous 
system have also been carefully studied, and show numerous 
variations in tvpe, the most important being the number and 
complexitv of the protoplasmic processes, and the division or 
even excessive branching of the neuraxon. The morbid changes 
that can be observed by the application of this stain are but few, 
since it appears that the pathologic cells soon lose their power 
of impregnation. Golgi and, in this country, Berkley have made 
the most extensive investigations by this method. It must be 



DISEASES OF THE BRAIN AND ITS . MEMBRANES. 753 



said, however, that in the majority of instances their studies were 
made upon the pyramidal cells of the cerebral cortex, and not 
those of the anterior cornna of the cord. 

Recently, Apathy and Bethe, by the employment of certain 
exceedingly complex staining methods, have claimed to have dis- 
covered that the nerve-cells are really nothing but stations in the 
paths of certain delicate fibrilla, called the neuro-fibrils, that pass 
from one cell to another, not being limited even to the ganglion- 
cells, but also passing through the neuroglia-cells. They there- 
fore believe, and Nissl has agreed with them, that these fibrils 
are the real functioning elements in the central nervous system, 
and that the ganglion-cells have probably only some nutritive 
influence. 

The alterations are essentially of two kinds : first, the appear- 
ance of varicosities upon the protoplasmic processes in their thicker 
branches ; second, the disappearance of the gemmules from the 
terminal filaments. Such alterations Golgi has seen in chorea, 
Nageotte in general paresis, and Berkley in alcoholism and other 
forms of poisoning. Sailer has found very marked changes of 
this character in the spinal cords of guinea-pigs killed with teta- 
nus-toxin, and Steele has described a varicosity upon the axis- 
cylinder in the cortical cell in an animal killed by diphtheria- 
toxin. Lenhossek appears to regard the varicosities of the proto- 
plasmic processes as the result of an accumulation of the chromo- 
philic bodies, and Kolliker states that they are merely artefacts, a 
view held by most zoologists. Sailer 1 has found very character- 
istic changes of this type in the brain of a guinea-pig that was 
apparently healthy and killed for histologic purposes. 

In 1885, Nissl described a method for staining the nerve-cells 
which, on account of its differentiation of the structures of the 
protoplasm, and the possibility that by it cells in any stage of 
degeneration may be stained, has yielded most valuable results. 
It consists essentially of staining tissue, hardened in alcohol, by 
one of the basic anilin-stains, such as thionin or methylene-blue. 
The cells of the anterior cornua show the irregular outline and 
the numerous protoplasmic processes as before. Throughout the 
protoplasm are small, irregular bodies, sometimes vacuolated, that 
take the basic stain intensely. They are arranged somewhat con- 
centrically around the nucleus, but at the points where the pro- 
toplasmic processes come off become spindle-shaped and turn 
into them, and are also found in the processes as spindles. Be- 
tween these bodies the cytoplasm refuses to take the stain, and 
is called the achromatic substance. Nissl and some others be- 
lieve that it has a delicate fibrillar structure, but this has not 
been positively determined. A cup-shaped portion of the proto- 
plasm remains clear, and is usually rather sharply delimited from 

1 Verbal communication. 



754 



TEXT-BOOK OF PATHOLOGY. 



the remainder of the cell. From this extends a long, faintly 
staining, undifferentiated neuraxon. The nucleus does not stain, 
but remains as a clear space near the center of the cell, contain- 




Fig. 348.— Normal and degenerated nerve-cells of the anterior cornua of the spinal 

cord ; X 600. 

ing a round, deeply staining, and usually vacuolated nucleolus, 
surrounded by a membrane with irregular thickenings (Fig. 348). 
It has been claimed (Kronthal) that these so-called chromophilic 
bodies do not exist in the living cell, but are the products of dis- 
integration. In 1893, De Quervain laid down the following cri- 
teria by which he recognized pathologic changes : (a) modification 
of the nucleus, (b) vacuolization of the nucleolus, (c) disappear- 
ance of the nucleus, (d) diminished staining-capacity, (e) swelling 
of the ganglion-cells, (/) fragmentation of the protoplasmic pro- 
cesses, (g) shrinking of the cell, (A) vacuolization of the proto- 
plasm. He does not consider enlargement of pericellular space as 
of pathologic significance, even when mononuclear leukocytes are 
found in it. It must be confessed that these criteria are not 
entirely adequate, nearly all of the changes described depending 
in part upon the length of time between death and the fixa- 
tion of the tissue and upon the methods of preparation. The 
course of the pathologic changes appears to be somewhat as fol- 
lows : The granules become first very irregular in distribution and 
somewhat finer, so that the concentric arrangement is no longer 
distinct. They may then diminish considerably in number, so 
that the cell as a whole appears very much paler ; finally, the 
protoplasm may become entirely clear, a small amount of baso- 
philic substance only remaining that is collected in irregular 
masses around the nucleus. This also may disappear, and the 
cell remain as an irregular, faintly and diffusely stained mass in 
the midst of the tissue. This series of changes is by no means 
the only one that has been described. Occasionally the chromo- 
philic granules seem to dissolve, although their capacity for stain- 
ing is unimpaired, resulting in deeply and diffusely staining cells 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 755 



without any apparent structure, excepting the vesicle in the situa- 
tion of the nucleus (pyknomorphous state). Nissl regards these as 
artefacts, and it is true that they are frequently found in tissues 
supposed to be healthy. It must not be forgotten that they are 
always far more numerous in diseased tissues or in the neighbor- 
hood of focal lesions. I have observed some singularly beautiful 
examples of this change in the brain of a guinea-pig killed by 
anthrax, in wdiich the micro-organisms were found in the nervous 
tissue. The solution, with or without loss of staining-power, cor- 
responds very closely to the changes observed in the chromatin in 
karyolysis, and may be very properly described as a sort of chro- 
molysis. In other cases chromophilic bodies may collect in diffuse, 
irregular masses in one or more parts of the protoplasm, a change 
which I have observed in the spinal cells of cases of tetanus. 

Still another form is the coalescence of the chromophilic bod- 
ies, so that each individual one appears larger; their number is 
less, and they still maintain a rather regular arrangement in 
the protoplasm. These masses may then further coalesce, giving 
rise to the appearance just previously described, or may break up, 
causing a uniform granulation of the cell, or they may disappear. 
Berger has attempted to explain most of these phenomena by sup- 
posing that the chromophilic bodies are really composed of small 
granules that are adherent to the sides of the spaces formed by 
the reticulum of the protoplasm of the cell. If these spaces 
dilate, the granules will be more widely separated and the appear- 
ance will be that of diffuse granulation. If they contract, as 
occurs in cases of general cellular contraction, the so-called in- 
spissation of the cell, they will appear darker and the neighboring 
ones may seem to coalesce. The changes in the reticulum may 




Fig. 349.— Degenerated nerve-cells in the neighborhood of a collection of pus ; the gran- 
ular appearance is due to an excess of pigment; X 600 tease of Lloyd and Sailer). 

be local, and give rise to local alteration in the arrangement 
(Fig. 349). 



756 



TEXT-BOOK OF PATHOLOGY. 



Another change that frequently occurs in pathologic cells is 
vacuolization. It is possible that a few vacuoles of small size 
may be the result of the hardening processes. In some cases, 
however, this alteration is very extensive, the vacuoles reaching 
70 jui in diameter. They appear to be filled with a liquid, possi- 
bly lymph, that may undergo slight coagulation-necrosis * at least 
fibrillar, that may be fibrin, have been observed. The cells often 
acquire extraordinary appearances. Indeed, it looks as if the 
pericellular space was enormously dilated, and that bands of pro- 
toplasm extend from it to the surrounding neuroglia. The 
arrangement of the vacuoles is always exceedingly irregular, and 
if more than one is present, as is usually the case, the vacuoles 
vary greatly in size. 

Sometimes, instead of the vacuoles, there may be found in the 
cells masses of some substance that differs from the protoplasm. 
These are usually homogeneous irregular masses that take the acid 
stain, and have been described as " colloid " in nature, using the word 
in the sense given to it by von Recklinghausen. The true nature 
of this change, however, is not very clearly understood. Some- 
times the vacuoles appear to be replaced by clefts distributed irreg- 
ularly in the protoplasm. 

In nearly all degenerated cells there is accumulation of a 
peculiar cellular pigment. This may be fatty in nature, as it 
stains black with osmic acid. In some cases it seems to increase 
pari passu with the disappearance of the chromophilic bodies, so 
that ultimately the cell appears as an irregular mass filled with 
this yellowish-brown pigment. It occurs normally in old age, is 
found in the cells of the substantia nigra of the crura, is an almost 
invariable accompaniment of those diseases in which a sort of early 
senility appears to occur, such as general paralysis, and is rarely 
found in cells undergoing very acute degeneration. Another 
form of pigment giving the iron reactions occurs in certain 
pathologic states. McCarthy has reported its occurrence in the 
brain of a rabbit killed by snake-venom. 

The changes of the nuclei first appear in the nucleolus ; this, 
as has been said, normally contains one or two vacuoles. In de- 
generative processes it begins to swell, and more vacuoles develop, 
so that finally it presents the appearance that has been likened by 
Berger to the morula stage of the ovum. Ultimately, as the de- 
generation progresses, it may grow fainter and disappear entirely. 
Clumps of chromatin are often observed at the periphery of the 
nucleolus, and occasionally ray-like fibers project from them into 
the nucleus ; accessory nuclei are also often present. Two or 
more nucleoli have also been observed, but it is doubtful if this 
is a morbid change, although Berkeley contends that it is an in- 
variable sign of irritation. 

The nucleus itself exhibits a variety of changes. Stained with 



DISEASES OF THE BE ATX AND ITS MEMBRANES. 757 



hematoxylin, it shows a delicate chromatin reticulum, and this may 
exhibit, in the ordinary forms of degeneration, changes that are 
found in other cells in the process of karyolysis ; occasionally the 
chromatin collects in a diffuse, irregular mass about the nucleolus. 
In various forms of degeneration the nucleus seems to be stimu- 
lated, and shows karyokinetic figures, or may even divide com- 
pletely, so that two nuclei are found in the same cell. This, how- 
ever, is not necessarily a degenerative change, because similar ap- 
pearances are found in embryonal and in lacerated nerve-tissue. 
Perhaps the most important nuclear change, and one that is 
most certainly pathologic in nature, is the dislocation of the 
nucleus. It may be found at the periphery of the cell, or even 
protruding from it, as if to be expelled. Wagner has even de- 
scribed nuclei lying outside the cells without nuclei ; but Berger 
suggests that in these cases the cells have become excessively 
vacuolated, and that the nuclei lie among the vacuoles, whose 
situation at the periphery of the cell causes it to appear smaller 
than it really is. I have never seen nuclei more than slightly pro- 
truding from degenerated cells. It has been said that the nucleus 
ean disappear from the cell when it does not present marked de- 
generative changes ; it must be remembered, however, that the 
large diameter of the multipolar cell renders it possible with a 
good microtome to make a number of sections through a single 
cell, and it is very likely that these conditions are due simply to 
sections beyond the plane of the nucleus. In the most advanced 
types of degeneration the nucleus certainly disappears completely. 

Changes may also take place in the cell as a whole. In the 
process of degeneration its outline usually becomes irregular and 
angular. The cell appears to be smaller, and often the pericellular 
space is very obvious. In many cases, however, this is an arte- 
fact, produced by the hardening fluid, and although it may be also 
the result of some morbid process, it is impossible to give it any 
value as such. In the early stages of degeneration the proto- 
plasmic processes may be unimpaired. A^aricosities, such as 
shown by the silver-impregnation, are rarely observed by the 
Xissl method. I have, however, seen them in the nerve-cells of 
the cord of a guinea-pig killed by tetanus. Tortuosity of the 
protoplasmic processes is very common, particularly in chronic 
conditions, such as sclerosis. It is impossible to stain the terminal 
ends by the Nissl method, and the changes in the gemmules can- 
not therefore be recognized. Sometimes the processes become 
friable, break off, and disappear completely, leaving the cells 
with a rounded outline. Finally, dislocation in the arrangement 
of the pyramidal cells of the cortex has been observed, particu- 
larly in cases of sclerosis of the brain, and it is probable that it 
occurs in all parts of the nervous system, although when the 
normal arrangement is irregular, it is impossible to estimate its 



758 



TEXT-BOOK OF PATHOLOGY. 



extent. Berger has recently called attention to a very peculiar 
appearance which may occur in degenerated cells. Sometimes in 
the portion of the nucleus opposite the nucleolus there is a small 
projection from the wall which passes inward toward the nucleo- 
lus, but before it reaches it, branches into three or four arms 
that have dilated ends. These seem to encircle the nucleolus, but 
are not directly in contact with it. He is unable to give a satis- 
factory explanation of this appearance, but suggests that perhaps 
it represents some form of duct conveying the secretion of the 
nucleus to the protoplasm of the cell, ordinarily unstainable, but 
in degenerated conditions filled with altered fluid. 

The functions of the different portions of the nerve-cell are but 
imperfectly known. The neuraxon conveys impulses from the 
cells to the periphery, or transfers them in some as yet inexpli- 
cable manner in a variety of directions along the collaterals. The 
cell-body has a distinct trophic influence over the neuraxon, and 
when this is removed, either by destruction of the cell or by the 
division of the neuraxon, the peripheral portion of the latter 
rapidly degenerates. On the other hand, the experiments of 
Goldscheider, Flateau, and Nissl have shown that the neuraxon 
exerts at least a temporary influence over the nerve-cell, and 
when it is destroyed in any way, pathologic changes invariably 
occur. There are many theories concerning the function of the 
nucleus, but no more is really known about it in the nerve-cell 
than in any other cell. It is concerned in active division, but 
this is apparently an exceedingly rare occurrence. The protoplas- 
mic processes have been regarded as nutritive or as centripetal 
organs. Lenhossek has suggested that the long axis-cylinders 
that convey impulses to the cells of the spinal ganglia are only a 
modified protoplasmic process. If this is so, it would be sufficient 
proof that they have an active function. The fact that the axis- 
cylinders of other cells terminate in arborization about the den- 
dritic processes, the cells forming the next link in the chain, is 
also a proof that even the short dendrites receive impulses. The 
fact that a single particularly thick dendrite may almost always 
be observed passing to the nearest blood-vessel indicates that they 
possess also some nutritive function, and that their extensive 
arborization is partly for the purpose of exposing as great a sur- 
face as possible to the nutritive fluid in which the cell is bathed. 
Concerning the pathologic physiology of the nerve-cells we have 
at present little information, although certain definite changes 
have been described, particularly by Hodge, in cells that have 
been exhausted by excessive stimulation. What changes occur in 
the cell preceding the production of energy have not yet been 
determined. 

The nerve-fibers are of two kinds, the medu Hated and the 
non-medullated. Non-medullated nerve-fibers consist of the axis- 



DISEASES OE THE BRAIN AND ITS MEMBRANES. 759 



cylinder alone. They are found in the olfactory nerve and in the 
sympathetic nervous system, and when they undergo degeneration 
exhibit swelling and varicosities, and ultimately break down into a 
granular detritus. Non-medullated nerve-fibers may also be pro- 
vided with a sheath, the neurilemma ; such fibers are found in 
some of the cerebrospinal nerves. Medullated nerve-fibers may 
consist only of the myelin-substance and the axis- cylinder — that 
is, the neurilemma is absent ; such fibers are found in the central 
nervous system. Ordinarily, they consist of the neurilemma, the 
myelin-substance, and the axis-cylinder ; such fibers are found in 
the central nervous system and in the peripheral nerves. These 
fibers may branch, either giving off collaterals in their course, or 
forming more or less complex aborizations at their terminations. 
The axis-cylinder usually exhibits a somewhat fibrillar structure. 
The myelin-material resembles fat and has a high refractive in- 
dex. It does not extend the whole length of the fibers, but, at 
rather regular intervals, is absent (nodes of Eanvier). These 
points are perhaps for the purpose of providing access for nutri- 
ment to the nerve-fiber. Upon the inner surface of the neuri- 
lemma are found a few oval nuclei surrounded by protoplasm. 

The function of the nerve-fibers is comparatively simple. Im- 
pulses are conveyed by the axis-cylinder, the neurilemma and the 
myelin substances apparently serving for protection and perhaps 
nutriment. It was formerly supposed that the myelin acted as 
an insulating material ; but the fact that non-medullated fibers 
exist shows that in some cases at least it is unnecessary for this 
purpose. 

The earliest symptom of degeneration in the nerve-fibers is the 
appearance of granules in the myelin-sheath. These soon run 
together and form droplets that give all the reactions typical of 
fat. Such a fiber, examined microscopically in longitudinal sec- 
tion, exhibits these droplets arranged irregularly along its course, 
giving rise to a somewhat beaded appearance. (Such axis-cylin- 
ders may be stained by osmic acid (Marchi's method), or by 
Sudan III., providing the tissue has not been hardened in alcohol.) 
The next change is usually found in the axis-cylinder. This may 
swell and become extraordinarily varicose, so that indeed it loses 
all resemblance to a nerve-fiber. Instead of being fibrillar, it has 
an irregular granular appearance, and may contain here and there 
minute droplets of fat, or the fiber may shrink and become granu- 
lar, and ultimately disappear, nothing remaining to indicate its 
previous existence excepting a mass of delicate granular detritus. 
These changes may be brought about, either by the destruction of 
the ganglion-cell from which the axis-cylinder forming the fiber 
arises ; or by separation of the fiber from its ganglion-cell ; or by 
injurious agencies acting locally upon the nerve-fiber. The second 
form of degeneration — that is,, taking place in the peripheral por- 



760 



TEXT-BOOK OF PATHOLOGY. 



tion of the cut nerve — is known as Wallerian. Changes in the 
proximal end also occur, but rarely extend further than the first 
node of Ranvier. When a nerve has been divided the earliest 
change is found on either side of the point of division, and con- 
sists in fragmentation of the myelin. About the third day fat- 
droplets appear in the myelin ; there is some swelling of the axis- 
cylinder ; and often proliferation of the nuclei in the neurilemma 
may be observed. As the myelin breaks down into a fatty detri- 
tus, it is gradually absorbed by the compound granular-cells, which 
appear all along the course of the nerve-fiber, and at the end of 
three or four months it has entirely disappeared. During this 
period the neuroglia is undergoing proliferation ; at first there is a 
slight increase in the number of neuroglia-cells ; later, the pro- 
liferation of the fibers preponderates, and, finally, the degenerated 
area is occupied by a thick mass of coarse fibers that usually 
undergo slight contraction. The proliferation of the cells ceases 
about the time that the fibers have become completely degen- 
erated. The subsequent proliferation, if any, occurs only in the 
neuroglia-fibers. The central portion of the separated fiber will, 
after a long interval, also degenerate : this is possibly due to 
functional inactivity, and appears to be more of the nature of an 
atrophy. Thus in amputations that have occurred in early life, 
the anterior roots, forming the nerves that supply the amputated 
limb, become smaller and contain fewer fibers, and there is ulti- 
mately some degeneration in the ganglion-cells of the anterior 
horns. Regeneration of nervous tissue occurs in the invertebrates 
and possibly among fishes and reptiles, although this is very un- 
certain. Regeneration of nerve-fibers in the peripheral nervous 
system occurs in all the higher animals, including man. After the 
nerve-trunk has been cut, the peripheral ends of the axis-cylinder 
of the central portion of the nerve become swollen and split up 
into very fine fibrillar. These grow in various directions, and, if 
they unite with the distal portion of the nerve, will use it as a 
skeleton, and one of them, at least, will grow toward the periphery, 
ultimately forming new nerve-fibers. These changes occur in both 
sensory and motor fibers. (See section upon the Regeneration of 
the Peripheral Nerves.) 

The neuroglia of the nervous system may proliferate or 
undergo softening, the former change producing various forms of . 
sclerosis or gliosis. Sclerosis of the brain may be either diffuse or 
circumscribed, and the latter is again subdivided into the hyper- 
trophic and atrophic forms. 

Diffuse sclerosis of the brain never involves all parts equally. 
To a certain extent it is normal in old age, and is usually found to 
be limited to the most superficial portion of the cortex beneath 
the pia, or else to the layer of the gray substance adjacent to the 
white matter. The neuroglia-tissue in either situation appears to 



DISEASES OF THE BRAIN AND ITS MEMBRA NES. 7 6 1 



be composed of rather coarser fibers than common, either forming 
wavy bands or a coarse network. Macroscopically the brains 
exhibit only slight alteration. The consistency may, on account 
of other senile changes, be even slightly reduced ; the gray matter 
is usually narrower than normal ; the pia mater is generally firmly 
adherent, but not invariably. This condition sometimes occurs in 
connection with other diseases, as epilepsy, or may be congenital. 

Disseminated sclerosis is sometimes only slight in extent. It 
may occur in the brains of epileptics, of criminals, of old persons, 
and of idiots. The small sclerotic foci are usually found at the 
junction of the gray and white matter, more particularly in the 
former than in the latter. The neuroglia-tissue forms a coarse, 
irregular network ; as a rule, it is unusually vascular and without 
any or only a few true nervous elements. These areas may be 
detected by the naked eye, when large enough, by the fact that 
they are paler than the surrounding tissue and often slightly 
sunken. If the process is more extensive and involves the whole 
thickness of one or more gyri, it gives rise either to the atrophic 
or hypertrophic form, or both may coexist in the same brain. The 
external appearance in these cases is characteristic, and cannot be 
mistaken for any other process. 

In the atrophic form the gyri are reduced perhaps to the thick- 
ness of a lead-pencil, they are pale, firm, slightly granular upon the 
surface and the pia mater may be slightly adherent ; but this is 
not common. Section through one of these convolutions shows 
that the cortex is considerably thinner and has a tendency to 
retract. The white substance is also involved, but apparently 
less severely. The extent of the process is very variable, 
one or two convolutions only being affected, or perhaps, as in 
several reported cases of epilepsy, only the cornua ammonis. 
Sometimes a number of convolutions are affected, and in the 
majority of* these cases there is some tendency to an irregularly 
symmetrical distribution. Microscopically these lesions show 
marked hyperplasia of the neuroglia-tissue — that is, increased 
number of neuroglia-cells and coarseness of the neuroglia-fibers, 
which form coarser meshes than usual. Many of the neuroglia- 
cells are swollen, the nuclei are enlarged, pale, and the out- 
lines of the cells are irregular. In some cases a number of the 
cells show a slight projection upon one side. The nervous elements 
may appear to be more thickly placed and somewhat irregularly 
distributed, and the protoplasmic processes of the ganglion-cells 
are often tortuous. More frequently they are considerably dimin- 
ished in number or else entirely absent. The myelinated fibers 
are always decreased, particularly the tangential fibers of the cor- 
tex. The vessels are more numerous than usual and often show 
wide perivascular spaces filled with fibrous tissue. In the most 
advanced areas, however, the vessels may be entirely absent. 



762 



TEXT-BOOK OF PATHOLOGY. 



Corpora amylacea or kindred products of nerve-degeneration are 
sometimes found. Ordinarily the neuroglia-fibers are arranged 
in bands just beneath the pia. Sometimes they form distinct 
whorls. These changes are usually found in epilepsy and idiocy, 
and when the lesions occur in the motor region are always asso- 
ciated with motor disturbances. 

In the hypertrophic nodular form, the brain, as a whole, is 
usually somewhat enlarged, and nodules are found in the cerebral 
cortex that project from the surface and are much harder than the 
surrounding substance. The larger ones are often slightly umbili- 
cated. The surface of these nodules is often granular. The micro- 
scopic changes are similar to those found in atrophic sclerosis, with 
the exception that the excess of neuroglia-tissue is much more 
pronounced. In these brains there are often sclerotic areas 
beneath the ependyma of the ventricles, the lateral ventricles 
being more frequently affected than the third or fourth. These 
nodules are small, round, and very hard. Microscopically they 
are found to consist of neuroglia-fibers arranged in a somewhat 
concentric manner. They may be vascular or entirely deprived 
of blood-vessels, and sometimes contain chalky deposits or masses 
of hyaloid material. As in all destructive lesions of the central 
nervous system, secondary degenerations may occur, but they are 
far less common than would be suspected from the apparent extent 
of the degenerative processes. These forms of congenital sclerosis 
probably commence after the seventh month of fetal life, because, 
as Kundrat has pointed out, the arrangement of the convolutions 
is rarely disturbed. They have been ascribed to syphilis, to in- 
flammatory change, to congestion of the lymphatic system, and as 
akin to tumor-formation. The absence of round-cell infiltration, 
and the fact that the pia is rarely adherent, even when the sclero- 
sis takes place in the most superficial layers of the cortex, would 
seem to exclude inflammatory causation. Neurogliar proliferation 
occurs about gumma, but there is no ground for believing that all 
other forms are also due to syphilis. The dilatation of the peri- 
vascular spaces is favorable to the theory of congestion of the 
lymphatic system. This, however, is probably secondary. It is 
no explanation for this process to say it belongs to the tumors, but 
at present it appears impossible to give a more satisfactory eti- 
ology. Softening of the neuroglia is a part of all processes of 
softening in the brain, which are described in connection with 
thrombosis and embolism. A condition that is possibly the result 
of softening during fetal existence, but may be a congenital mal- 
formation, and consists of the formation of cavities in the brain, 
may properly be described here. 

Porencephaly is a condition characterized by the absence of 
a greater or less amount of the substance of one or both of the 
cerebral hemispheres, leading to the formation of a cavity or cav- 
ities filled with cerebrospinal fluid. 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 763 



Etiology. — The cause of porencephaly is not definitely ki.own. 
As Von Kahlden remarks, the similarity of the lesions in typical 
cases is such that it seems reasonable to accept a uniform etiology. 
Kundrat believed that the lesions were due to anemic infarction, 
as a result of the occlusion of the Sylvian arteries. Freund also 
accepts this as the cause in a certain number of cases. Von 
Kahlden, however, believes that it is the result of some disturb- 
ance in a development of the brain, and bases his opinion upon 
the symmetry of the lesions and their peculiar situation. Other 
authors have suggested an inflammatory origin of the process, 
because of the adhesions between the membranes. A certain num- 
ber of cases certainly develop after birth ; these may be due to 
injury, such as might be produced by instrumental delivery, or by 
blows upon the skull, or by embolic or inflammatory processes. It 
can only be said, however, that the etiology is at present unknown. 

Pathologic Anatomy. — Von Kahlden has divided the cases 
hitherto reported into two classes : the typical and the atypical. 
The former class comprises about two-thirds of all the cases, and 
is characterized by the presence of a funnel-like cavity in the 
motor region of the brain, usually bilateral, although unequal, that 
extends from the subarachnoid space to the cavity of the ventricle 
(Fig. 350). Frequently this condition is associated with imperfect 
development or exposure of the island of Reil. In the atypical form 
the lesions are exceedingly various ; they may be found in any part 
of the cerebral hemispheres ; the shape of the cavity may be either 
a shallow depression or a considerable loss of substance. Often — 




Fig. 350.— Porencephaly (case of Dr. J. H. Lloyd). 

in fact, usually — there is no communication between the cavity and 
the ventricle. These varieties may even be found in the cerebel- 
lum, and perhaps are most frequent in the lateral lobes at the point 
where they unite with the vermiform process. Cases have also 



764 



TEXT-BOOK OF PATHOLOGY. 



been recorded with cavity-formation in the base of the brain, com- 
municating sometimes with one of the horns of the lateral ventri- 
cles. A sort of cystic formation has been described, in which 
multiple cavities, not communicating with either the ventricle or 
subarachnoid space, have been found in the substance of the brain. 
The macroscopic changes observed in the typical form are as fol- 
lows : ordinarily a distinct depression is noticed in the dura after 
the skull has been removed. When this region is more carefully 
examined it is found that the dura may or may not be adherent 
to the arachnoid which covers the cavity. The pia usually dips 
into and covers the wall, and may be continuous with the epen- 
dyma of the ventricle. The adjacent convolutions of the brain 
are arranged in a somewhat radiate manner and turn down into 
the cavity, although this is not invariably the case, for they some- 
times may appear as if simply cut off, being otherwise normally 
arranged. Associated changes in the brain are microgyria ; pro- 
liferation of the neuroglia-tissue, and perhaps also of the con- 
nective tissue ; atrophy of the nerve-cells in the cortex, particu- 
larly of the large pyramidal cells ; and more or less complete 
destruction of the nerve-fibers in the region adjacent to the defect. 
Rarely there is a sort of cystic degeneration of the walls of the 
cavity. The spinal cord usually exhibits a secondary degen- 
eration in the pyramidal columns ; this, however, is not always 
the case, for sometimes it appears that one or both pyramidal 
columns have failed entirely to develop, giving rise to a condition 
of micromyelia. Other parts of the brain appear to be rarely 
affected in the typical form of the condition. When the lesion 
is situated in any other part than the central region, corresponding 
secondary degenerations may, of course, occur. 

THE BLOOD=VESSELS. 

The arteries of the brain may be divided into two groups, 
those nourishing the cortex and those nourishing the basal gan- 
glia. The former are the ramifications of the terminal branches 
of the circle of Willis ; the latter arise directly from the main ves- 
sels of the base of the brain. 

Atheroma. — The changes that occur in the arteries are those 
ordinarily occurring in the vessels of the other parts of the body, 
atheroma of the arteries of the base of the brain being perhaps 
more frequent than of the arteries of the majority of other organs. 
These atheromatous changes usually lead to calcareous infiltration, 
and in old age often the entire circle of Willis is composed of 
typical pipe-stem arteries. When the process is less extensive, 
the calcareous infiltration is most apt to affect the two internal 
carotids, the middle cerebrals, and the basilar artery. 

Hyaline degeneration may also occur. It is of two kinds : 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 76') 



that which forms simply the early stage of arterial sclerosis, and 
another process that is apparently independent of this, and occurs 
as a diffuse degeneration of the intima and media. This latter 
form is frequently found in the brains of chronic idiots even dur- 
ing early life. Occasionally it is also found in senile brains, but 
in these cases is not so certainly independent of arterial sclerosis. 
Amyloid degeneration of the blood-vessels may occur as a part of 
general amyloid disease, but is not especially common in the brain. 

Colloid Degeneration. — A rare form of degeneration has 
been spoken of as colloid, although the material discovered in the 
blood-vessels seems more akin to that of hyaline degeneration. In 
this process the adventitia and the media are greatly thickened as 
a result of their infiltration with a homogeneous translucent mate- 
rial, which may be deposited irregularly in masses, or else cause a 
diffuse thickening of the wall. The masses project into the sur- 
rounding nervous tissue, and may sometimes be detached, forming 
then independent clumps that are not unlike the so-called amyla- 
ceous bodies, although they fail to give all the characteristic amy- 
loid reactions. This condition is usually associated with profound 
disturbances of the intellect, and may give rise to clinical symp- 
toms that resemble those of general paresis. A case of this nature 
has been reported by Alzheimer. This colloid or hyaloid material 
is soluble in boiling water and in alkaline solutions. It stains a 
bright-red by Van Giessen's method, and usually blue by Wei- 
gert's fibrin-method. Sometimes it stains brown with iodin, but 
not invariably. There is usually extensive degeneration of the 
nervous elements, which may be associated with secondary changes 
in the spinal cord. 

Injury followed by softening of the brain causes considerable 
thickening of the walls of the blood-vessels, which seems to be 
due chiefly to proliferation of the intima ; but there is also dis- 
tinct proliferation of the media. As a result, the lumen is con- 
siderably decreased. These changes occur in all the blood-vessels 
throughout the affected area. 

Syphilis frequently causes thickening of the intima or endarte- 
ritis, which may be due either to the usual round-cell infiltration 
or to the formation of fibrous tissue. Tuberculosis may also cause 
endarteritis. This form is most frequently associated with tuber- 
cular meningitis, and therefore the basilar artery is the one most 
frequently affected. 

Aneurysms may occur in any of the components of the circle 
of Willis. The basilar artery is the one most frequently involved, 
usually just at its posterior extremity. Large aneurysms of the 
arteries of the brain proper, or of the arteries of the vertex, are 
exceedingly rare. A saccular aneurysm, as large as a cherry, 
springing from the anterior communicating artery, was observed 
at the Philadelphia Hospital. Miliary aneurysms of the brain are, 



766 



TEXT-BOOK OF PATHOLOGY. 



on account of their etiologic relation to cerebral hemorrhage, the 
most important form of vascular disease in the brain (see Fig. 182). 
These aneurysms may be ectatic or saccular. The ectatic forms 
are usually fusiform in shape, and often consist of but a single coat 
of the vessel-wall ; that is to say, they are merely endothelium 
surrounded by a thin layer of fibrous tissue. The saccular aneu- 
rysms are usually somewhat larger ; they appear as bulbous swell- 
ings on one side of the vessel, connecting with the lumen by nar- 
row openings. They may consist of a single wall, as in the fusiform 
type, the most common variety, or of the intima or adventitia, with 
a considerable amount of fibrous thickening. Occasionally the 
fusiform aneurysms may exhibit distinct atheromatous change, but 
even in these instances the media is atrophic, and they are certainly 
exceptional. It is doubtful whether arteriosclerosis is of much 
importance in connection with the formation of these aneurysms, 
and it is certain that in the majority of cases the first change in 
the vessel is a fatty degeneration of the media. This leads to local 
weakening of the wall and to consequent distention — a change that 
is favored by the considerable degree of pressure to which the 
arteries springing from the middle cerebral or from the beginning 
of the basilar artery are subjected. According to some authors, 
these aneurysms are to be regarded as hernia? of the intima, really 
the result of atrophy of the muscularis, nevertheless they are more 
frequent in the old, and certainly in the majority of cases in which 
they are found, the arteries of the base are distinctly atheromatous. 
The formation of thrombi in miliary aneurysms is exceptional. 

CIRCULATORY DISTURBANCES. 

Circulatory disturbances in the brain differ from those in other 
parts of the body on account of the presence of a rigid bony cap- 
sule (the skull), which prevents any increase or decrease in the 
size of the contained viscus. Variations in the quantity of blood, 
however, do take place in adults, and are rendered possible, first, 
by the elasticity of the nervous substance itself, which is capable 
of undergoing a slight degree of compression or extension, and, 
second, by the free communication of the subarachnoid spaces of 
the brain and cord and the ventricular cavities, so that the cere- 
brospinal fluid may. be in greater or less quantity in the cavity 
of the skull or in the spinal canal, and thus permit variation 
in the amount of blood in either region. Local congestion or 
anemia may occur as a result of local disturbances, but the free 
anastomosis of the arteries of the circle of Willis provides such 
facility in equalizing the amount of blood flowing to the different 
parts of the brain, that neither is often found in general condi- 
tions. In very young children these mechanical restrictions do 
not obtain, because the fibrous union between the bones of the 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 767 



skull permits of very considerable changes in the size of the 
cranial cavity. 

Acute anemia of the brain may occur as a result of severe 
hemorrhage, or of hyperemia in other parts of the body, particu- 
larly the pulmonary and abdominal organs, and it has been sup- 
posed to exist in fainting, during hysterical crises, and in sleep. 
It must be admitted, however, that certain proof of its existence 
either as a cause or effect of the three latter conditions is lacking. 
Microscopically the brain is usually pale and firm. There is little 
or no tendency on the part of the small venules of the white sub- 
stance to bleed upon cross-section, and the gray matter is dis- 
tinctly paler, so that the distinction between it and the medullary 
substance is not so distinct as is the case in normal tissue. Some- 
times in these conditions there is overfilling of the veins of the 
pia as a result of the shrinking of the brain. The changes in the 
functions of the brain-tissue ascribed to this condition are partly 
irritative, partly paralytic. They are very indefinite. 

Chronic anemia of the brain may occur in severe cachectic 
conditions, such as progressive pernicious anemia, lead- or malarial 
poisoning. It may also be the result, though less frequently, of 
atheroma of the cerebral arteries, with a general narrowing of 
their lumina. The brain is small, the consistency varies accord- 
ing to the duration and nature of the process, being at first hard, 
later, probably as a result of degenerative changes, slightly softer 
than normal. The ventricles are not dilated at first, but the con- 
volutions are shrunken and the sulci are wider as a result of the 
diminution in size of the brain as a whole. The substance of the 
brain is pale, and often seems slightly moister than normal. Local 
anemia may occur as a result of thrombosis or embolism, and 
usually leads to softening. 

Active hyperemia of the brain is nearly always associated 
with inflammatory or toxic conditions. It is perhaps most fre- 
quent in association with meningitis or encephalitis. It is always 
found after death from sunstroke, acute delirium, cholera, and 
hydrophobia ; as well as, occasionally, after death from infectious 
disease. It may be local or general. 

Local hyperemia is usually associated with meningitis, and 
may be limited to the superficial layer of the cortex beneath the 
meningitic areas. The affected parts are darker than normal and 
may even contain punctiform hemorrhages. Microscopically the 
blood-vessels are found to be dilated, and there is more or less 
degeneration of the adjacent nerve-substance, according to the 
duration of the process. Local hyperemia may also occur after 
thrombosis, and leads to red softening of the nerve-tissue. 

General active hyperemia is supposed to be associated with un- 
usual activity of the mind, particularly prolonged and intense 
mental effort. Certain proof of this, however, has not yet been 



768 



TEXT-BOOK OF PATHOLOGY. 



furnished. The brain is darker and larger and its consistency is 
softer. The blood-vessels of the pia are injected. The gray mat- 
ter is darker and, as in the local form, may contain minute hemor- 
rhagic foci. The white matter is moist; its color is rarely altered, 
but as soon as the section is made it is covered with small red 
spots, representing hemorrhages from the veins and capillaries. 
These may be readily distinguished from interstitial hemorrhages by 
allowing a little water to flow over the surface of the section, when 
they will disappear. Microscopically, aside from the distention 
of the vessels with blood, pronounced degenerative changes are 
rarely found, excepting in those cases resulting from infectious 
diseases. In these the alterations commonly associated with severe 
toxemia are present, but are to be considered as complications, and 
not as the result of the circulatory disturbances. 

Occasionally, in acute infectious diseases such as typhoid fever, 
a condition occurs in which there is evidently excessive irritation 
of the central substance, manifested by symptoms not unlike those 
of meningitis. Post-mortem in these cases the only changes 
found are hyperemia of the brain. Even microscopically no dis- 
tinct inflammatory lesions can be discovered. This condition has 
been termed meningismus. 

Passive hyperemia may be associated with valvular heart- 
disease or chronic lung-disease, or it may be caused by tumors 
in the neck pressing upon the jugular veins, or by intracranial 
conditions. Of the latter, the most important are brain-tumors 
compressing the veins, whilst the arteries still continue to con- 
vey blood, and thus cause increase of the cranial contents. 
When the tumors press upon the veins of Galen passive hyper- 
emia and distention of the ventricles are particularly common. 
Passive hyperemia may also be caused by thrombosis of the dural 
sinuses. In acute passive congestion the veins of the dura are 
widely distended ; the subarachnoid space is moist ; the brain 
seems to be slightly larger, softer and moister than normal. The 
gray matter is of a slaty color. The white matter may have a 
faint bluish tinge, and its capillaries and ventricles bleed freely 
upon cross-section. The ventricles may not be larger, but appear 
to contain fluid under pressure, that wells forth when they are 
opened. 

Edema of the brain nearly always occurs when passive hyper- 
emia persists. This is characterized by the distention of the sub- 
arachnoid space with liquid, so that the convolutions are no longer 
distinct, and the surface of the brain has a clear or pearly appear- 
ance. The arachnoid is usually thicker, particularly along the 
sulci. The fluid is clear, or perhaps very slightly turbid ; it has a 
higher specific gravity than the cerebrospinal liquid, coagulates 
upon boiling, and is usually found to contain numerous cellular 
elements. A microscopic examination of the brain and its 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 



769 



membranes shows marked distention of the subarachnoid space, 
which is usually divided into irregular spaces by delicate fibrous 
bands. The endothelial cells appear to have undergone some pro- 
liferation, and in many places have desquamated and lie free in the 
areolar spaces. Around the blood-vessels there is occasionally 
slight extravasation of round cells, which are usually mononuclear 
and resemble lymphocytes, and indicate an inflammatory reaction 
to the long-continued pressure. The arachnoid is usually thicker,, 
the thickening being almost exclusively fibrous in nature. The 
pia is slightly thicker, and sometimes may be seen to have coalesced 
with the superficial layer of the cortex. In the brain-substance 
the perivascular spaces are distended, the neurogliar mesh work is 
coarser than normal, and there may be slight evidences of degen- 
eration in the cells. 

Local edema of the brain, the so-called apoplexia serosa, is 
occasionally found in the neighborhood of areas of softening. In 
cases of acute hydrocephalus this serous infiltration sometimes 
occurs in the neighboring internal capsules, and may even lead 
to transient hemiplegia. 

Cerebral hemorrhage occurs in two varieties : the so-called 
punctate form, and massive hemorrhage. 

Punctate hemorrhages are due to some alteration of the vessel- 
walls or of the degree of blood-pressure, causing extravasation 
of blood into the surrounding tissues. The hemorrhages are 
small, often microscopic, and are by far most common in the gray 
matter, especially in the cortex. The principal causes are hy- 
peremia, particularly if associated with inflammatory conditions 
of the brain, or convulsions. The wall of the blood-vessel may 
be diseased, but does not always show solution of continuity. The 
blood-pigment is more or less altered, according to the length of 
time that has elapsed between the occurrence of the hemorrhages 
and the examination of the tissues. The nervous tissue immedi- 
ately involved is edematous, and there is usually some prolifera- 
tion of the neuroglia-cells in the vicinity. Such hemorrhages, of 
course, may heal without leaving any trace, for the secondary de- 
generations that may possibly be caused are too slight to be 
detected. 

Massive hemorrhages usually occur from the branches of the 
middle cerebral artery — that is, from the vessels most frequently 
the seat of miliary aneurysms. They may also, however, occur 
in the centrum ovale or the pons, or, in fact, in almost any portion 
of the central nervous system. The blood usually collects in the 
form of an irregular dark-red mass that, in recent cases, rapidly 
becomes bright red upon exposure to the air. The size of the 
hemorrhagic area naturally varies with its location and the amount 
of blood extravasated. Its outline is exceedingly irregular, and 
almost always small separate hemorrhagic foci are found in the 

49 



770 



TEXT-BOOK OF PATHOLOGY. 



surrounding tissue. According to the density of the tissue, the 
blood is more or less dispersed. Thus, in the white matter the 
extravasation is usually more diffuse than in the gray, where hem- 
atomata are exceedingly apt to form. The substance of the brain 
is soon softened. Its structure is usually entirely lost, although 
it may be possible in recent cases to recognize the presence of 
altered cells and nerve-fibers. The neuroglia usually shares in 
this softening ; but if the hemorrhage is not extensive, it may 
remain and form a sort of skeleton ; the tissue then is not 
nearly so soft, and the surface upon section usually is smooth. 
If the hemorrhage occurs in the internal capsule, as is usually 
the case, and is at all extensive, the blood may creep inward 
toward the ventricle, into which it may rupture, filling the 
lateral ventricle, and sometimes extending into the third ventricle 
and into the lateral ventricle on the other side (Fig. 351). Oc- 




Fig. 351.— Hemorrhage into the internal capsule and the caudate and lenticular nucleus 
of the right cerebral hemisphere (from Bollinger). 

casionally, in exceedingly severe cases, almost the whole of one 
of the hemispheres may be destroyed ; this is usually associated 
with sudden death, and is known as the foudroyant form of apo- 
plexy. The softened brain-substance can usually be readily washed 
away by a current of water, leaving the blood-vessels, which 
should then be examined with a low power for the presence of 
miliary aneurysms. If the patient survives his first attack, rapid 
alterations begin to take place in the diseased tissue. The throm- 
bus contracts, causing edema in the surrounding tissues. A cap- 
sule of delicate fibrous tissue may even be formed about it. The 
small hemorrhages in the surrounding tissue are absorbed. The 



DISEASES OF THE BRAIN AND ITS MEMBRANES. Ill 



color of the softened region becomes dark brown, and it may 
either go on to complete liquefaction, with the subsequent absorp- 
tion of the pigment and the formation of a cyst, or else be gradu- 
ally entirely absorbed, leaving a pigmented scar. The walls of 
the cysts are usually discolored by pigment, and in the neighbor- 
hood pigment-granules and compound granular cells are found in 
great numbers. These old hemorrhagic cysts are very difficult to 
distinguish from those produced by other forms of softening. 
Often the contents are slightly discolored, the walls are dense and 
somewhat sclerotic in nature, and may contain crystals of hema- 
toidin. It is somewhat doubtful whether the walls are composed 
of neurogliar tissue or of true fibrous connective tissue derived 
from the blood-vessels. It is certain, however, that shortly after 
extravasation of the blood, hyperplasia of the neuroglia in the 
immediate vicinity takes place. This may occur very rapidly, so 
that in the course of a few days new neuroglia-fibers may be seen 
pushing their way into the hemorrhagic area from the collection 
of neuroglia-cells in the nearest healthy tissue. After healing has 
taken place the hemisphere is usually reduced in size. This re- 
duction is not merely equivalent to the amount of nerve-tissue 
that has been destroyed, but represents also the secondary degen- 
eration that occurs in the nerve-fibers whose course has been in- 
terrupted by the lesion. This is both ascending and descending, 
and frequently causes sclerosis that involves not only the brain, 
but extends throughout the pyramidal columns. 

Pathologic Physiology. — The disturbances in the functions of the 
central nervous system produced by hemorrhage are among the 
most interesting in the domain of nervous physiology. At the 
time of the rupture of the vessel the patient almost invariably 
becomes suddenly unconscious and falls, the face is flushed, and 
there may be convulsive movements. This is termed apoplexy. 
The period of unconsciousness may persist for a longer or shorter 
interval, according to the amount of hemorrhage that has taken 
place. If the patient recovers, the subsequent changes depend 
upon the situation of the hemorrhage and the extent of the de- 
struction of nervous tissue that has taken place. As will readily 
be seen from the description of the pyramidal tract, lesion in any 
part of its course above the first cervical segment produces paralysis 
of the opposite side of the body ; if above the middle of the pons, 
paralysis of the lower portion of the face on the opposite side is 
also produced ; if below this point, paralysis of the same side. 
Monoplegias are likely to occur if only a small portion of the 
fan-like projection-fibers of the pyramidal tract is involved, such 
as would be produced by a lesion in the cortex or in the centrum 
ovale. In all these cases only the superior motor neuron is 
affected, and in consequence, either because some inhibitory in- 
fluence is removed or because the lower motor neurons are 



772 



TEXT-BOOK OF PATHOLOGY. 



irritated by the products of degeneration, a condition of spasticity 
arises in the muscles. Subsequently, their nutrition is impaired 
and they contract. An interesting series of disturbances is pro- 
duced by lesions occurring in those portions of the cortex that 
have to do with manifestations of speech, either receptive or 
motor. If the former are involved, Ave speak of it as amnesia ; 
if the latter, as aphasia. Lesions of the optic tract posterior to 
the chiasm cause hemianopsia. 

Secondary Degeneration after Hemorrhages. — As a result of hem- 
orrhage into the brain-substance with destruction of tissue, second- 
ary degenerations appear, which, of course, are systemic and fol- 
low the direction in which the nerve-fibers convey impulses. Of 
these the most important are the degenerations of the pyramidal 
tract, of the optic tract, and of the projection-fibers from the 
temporo-sphenoid lobes. A discussion of this subject involves 
consideration of the anatomy of the brain more than of the pathol- 
ogy, and only the most important details can be given here. De- 
generation of the pyramidal tract may be sharply circumscribed if 
the focal lesion is situated in the cortex or the centrum ovale. In 
this case a slender band of degenerated fibers may be traced along 
the pyramidal tract. This is only possible, however, if the lesion 
is sufficiently recent to permit the employment of Marches stain- 
ing-method, for otherwise it is impossible to recognize a small 
number of degenerated fibers in the midst of a group of healthy 
ones. As the hemorrhage usually takes place from the lenticulo- 
caudate artery and involves the complete destruction of the pyram- 
idal fibers in the internal capsule, it not unfrequently happens 
that the entire pyramidal column of one side undergoes secondary 
degeneration. Hoche, who has recently studied two cases of 
cerebral hemorrhage, involving complete destruction of the motor 
fibers on one side, by Marchi's method, has found a rather pe- 
culiar distribution of the motor fibers in the crusta. Dividing 
this region into five parts, he finds that the two median sections 
are free from degenerated fibers. The middle section is almost 
completely degenerated, and there is also an area of degeneration 
in the median part of the fourth section, extending partly into the 
fifth. Degenerated fibers can also be traced going to the nucleus 
facialis of the opposite and the same sides, and to the nucleus 
hypoglossus of both sides. There were also degenerated fibers in 
the lateral pyramids of the same side. Interruption of the fibers 
of the optic radiation, or destruction of the primary optic centers, 
causes secondary degeneration which does not, however, appear as 
promptly as in the motor fibers. There is degeneration in the 
external geniculate body, in the pulvinar, and in the anterior 
corpus quadrigeminus of the same side. Ultimately, degenera- 
tion may also occur in the optic nerves. Destruction of the 
second and third temporal lobes, or of the projection-fibers aris- 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 773 



ing from them, causes secondary degeneration in the posterior 
limb of the internal capsule. The fibers appear to extend into 
the thalamus, and also into the crusta. Destruction of other parts 
of the brain-cortex causes degeneration, which seems to affect 
chiefly the projection-fibers. Extensive hemorrhages into the 
cerebellum usually cause death, as a result of pressure upon the 
medulla. If, however, the patient survives, and if the nucleus 
dentatus is particularly involved, there is degeneration of the 
superior cerebellar peduncle, which may be traced as far as the red 
nucleus in the tegmentum. Degenerations have been produced 
experimentally in the other peduncles. All these secondary de- 
generations are quite typical in character. They appear about the 
ninth day, the first changes being the degeneration of the myelin- 
sheath. This is followed by the appearance of compound gran- 
ular cells and hyperplasia of the neuroglia, and later corpora 
amylacea may sometimes be found. Ultimately nothing but the 
neuroglia remains, and this is composed of coarser fibers than are 
found in normal nervous tissue. Occasionally nerve-fibers without 
myelin-sheaths are. found traversing the sclerotic tissue. 

* Thrombosis and embolism of the vessels of the brain are 
due to causes that produce the same processes in other parts of the 
body. Thrombosis may occur anywhere. It is perhaps more fre- 
quent in the basilar artery than in other situations, but this rule 
is by no means certainly established. The causes are, of course, 
chiefly atheroma of the vessels or syphilitic endarteritis. Embo- 
lism, on the other hand, usually occurs in the artery of the Sylvian 
fissure. Perhaps 80 per cent, of all cases occur in this situation. 
Less frequently, an embolus will lodge in the anterior cerebral, 
but it is probably extremely rare for an embolus to travel along 
the posterior communicating artery and lodge in the posterior cere- 
bral. A more frequent route of embolism into the latter artery is 
along the vertebrals to the basilar. Embolism in the basilar artery 
can, of course, never occur, as its lumen is greater than that of 
either of the branches from which it receives blood. A saddle-embo- 
lus may occasionally lodge at its bifurcation and give rise to local 
thrombosis. Sometimes the two processes occur simultaneously — 
that is, fragments of a parietal thrombus in one of the vessels may 
be washed off into the blood-stream and be carried along the 
artery until they occlude its lumen or that of one of its branches. 
The results of embolism or thrombosis may be either infarction, or, 
if the obstruction takes place slowly, as in thrombosis, and it is 
possible for a collateral circulation to be established, there may be 
no changes, or such only as are temporary. 

Infarction of the brain usually leads very rapidly to cerebral 
softening (encephalomalacia). It has been usual to describe three 
forms of this — red, yellow, and white softening. 

The functional disturbances are very similar to those of hemor- 



774 



TEXT-BOOK OF PATHOLOGY. 



rhage. As, however, the lesions frequently occur very slowly, 
the sudden shock may not occur, and the paralysis may supervene 
without any period of unconsciousness. 

Red softening corresponds very closely to the hemorrhagic 
infarct. It consists of a serous infiltration of the tissue, the ex- 
travasated liquid containing numerous red corpuscles. The same 
theories that have been suggested for the explanation of a hemor- 
rhagic infarct have been used to explain its occurrence. 

Yellow softening is really only the red softening after more 
complete liquefaction has taken place and most of the pigment 
has been absorbed. 

White softening is a term applied to two very different 
conditions. The first corresponds to the anemic infarct, and 
appears very shortly after the occlusions of the vessels. The 
second is a late stage of any form of softening, and is character- 
ized by the formation of an excessive amount of fat in the softened 
area, producing an emulsion. The white color becomes even more 
pronounced after the fat has been absorbed, and the lesion is rep- 
resented only by coarse neuroglia-fibers. Macroscopically the 
earliest changes usually appear toward the end of the first twenty- 
four hours. The brain-substance in the softened area is swollen, 
softer, and somewhat mottled in appearance and may even exhibit 
small punctiform hemorrhages. The lesion is not sharply delim- 
ited, but fades gradually into the surrounding tissues. 

If a large artery has been obstructed, a considerable portion of 
the brain may be softened and there will be a large extravasation 
of blood. In this case, the parts of the brain showing the great- 
est alteration are those nearest the periphery of the distribution 
of the obstructed vessel, and these changes may even occur with- 
out complete obstruction if the general circulation is impaired, as 
in valvular heart-disease, or as a result of profound general 
anemia. As the process continues, more and more blood is ex- 
tra vasated into the tissue, giving it a bright-red appearance. The 
lesion by this time becomes more circumscribed, although the sur- 
rounding tissue may be somewhat softened, and, as in the case of 
hemorrhage, may contain punctiform hemorrhages. As soon as 
the demarcation is complete, the brain-tissue becomes rapidly 
softer, probably as a result of the obstruction of the lymph-chan- 
nels by which the nutritive fluids enter. The nerve-cells undergo 
almost complete degeneration ; they lose their axis-cylinders and 
their tinctability, and may either disappear completely or be no 
longer recognizable. The myelin-sheaths undergo a fatty degen- 
eration, in which the nerve-fibers soon take part. The whole 
tissue is filled with compound granular cells. The neuroglia- 
fibers may also become softened and, to a large extent, liquefied, 
although they persist longer than the other elements. The wall 
of what has now become a cyst is composed of the surrounding 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 775 



neurogliar tissue, newly formed capillaries, and nervous tissue in 
an advanced stage of degeneration. The blood-vessels, however, 
usually persist for some time, although they are filled with thrombi 
and form an irregular spongy network in the lesion. 

When organization commences the blood-pigment gradually 
disappears, and the material changes from a brownish, turbid fluid 
to a lighter yellow mass, often irregularly surrounded by deeply 
pigmented cells. Later, complete contraction takes place, and a 
scar, composed chiefly of neuroglia-tissue, but also containing some 
fibrous connective tissue that has developed from the walls of the 
blood-vessels, is left. It is, of course, clear, that red softening is 
more frequent in the vascular parts of the brain, and white soften- 
ing in those regions that are poorly supplied with blood, particu- 
larly in the white substance of the cerebrum. The areas are rarely 
as well circumscribed as those of red softening, and often do not 
lead to complete destruction of the tissue, causing only numerous 
adjacent minute focal lesions, the so-called etat crible. 

A peculiar form of softening occurs in the cortex of the brain. 
It is usually found as lesions that have existed for some time. 
The area is yellow, depressed, and somewhat circumscribed. The 
pia mater over and around the lesion is somewhat thickened, and 
often the surrounding blood-vessels show thickening of the walls, 
although this latter change is probably the cause and not the result 
of the changes. These are the so-called plaques jaunes of French 
writers, and if extensive they lead to considerable retraction of 
the brain-substance and to the formation of collections of liquid 
in the subarachnoid space {hydrops ex vacuo; external hydro- 
cephalus). 

Areas of softening, probably due to capillary thrombosis, are 
frequently found in children suffering from tubercular meningitis. 
They may also occur in other forms of meningitis, and also in 
encephalitis, although in these latter conditions the presence of 
pyogenic micro-organisms in the emboli lead to somewhat differ- 
ent changes, which will be described in connection with enceph- 
alitis. Traumatism may also cause softening, often multiple in 
character, and not necessarily situated directly beneath the point of 
injury. As a result of the destruction of tissue, secondary degen- 
erations occur that differ in no respect from those following hem- 
orrhage. 

INFLAMMATION. 

Encephalitis, or inflammation of the brain-substance, 

is probably not essentially different from inflammation of the other 
tissues in the body. The nature of nervous tissue, however, and 
the peculiar reaction that it manifests to various injurious agencies, 
render this subject one of the most doubtful and difficult in the 
pathology of the central nervous system. The various forms may 



776 



TEXT-BOOK OF PATHOLOGY. 



be classified, first, as acute and chronic. The important forms of 
acute encephalitis are the parenchymatous, the simple, the hemor- 
rhagic, and the suppurative. Chronic encephalitis may take the 
form either of sclerosis or of scar-formation, which is really only 
a modification of the former. Acute encephalitis may be consid- 
ered to be invariably disseminated or focal. No case has been re- 
corded in which there was extensive inflammatory change in the 
brain, and it is inconceivable that such a condition should be com- 
patible with life. 

Acute parenchymatous encephalitis is rather a form of degen- 
eration than a disease. Changes in the nerve-cells without associ- 
ated vascular phenomena have, in the last few years, been observed 
and described in a number of intoxications, either the result of 
poisoning or infection ; thus Berkeley has carefully studied the 
changes in the brain in alcoholic poisoning. More or less exten- 
sive changes have also been recorded as a result of poisoning by 
malon nitrite, arsenic, and other poisonous substances. Of the 
infectious diseases that have been studied, the most important are 
diphtheria, tetanus, leprosy, and hydrophobia. The changes differ 
somewhat in nature, and, of course, in the different cases, consid- 
erably in degree. The most important and typical have been 
already described in the section upon degeneration of the nerve- 
cells. These forms of encephalitis, if the name may properly be 
applied to them, may lead to death, but recovery even from the 
advanced stages is not impossible, as has been indisputably proved 
by the experimental research of Goldscheider and Flatau. Neither 
the brain nor the cord in these cases exhibits any macroscopic 
changes, excepting, perhaps, passive congestion of the membranes 
when death was preceded by violent convulsions, as in tetanus. 

Simple acute focal encephalitis is characterized by the develop- 
ment, in various parts of the brain, of areas of softening that may 
range from a millimeter to several centimeters in diameter. They 
are usually irregular in size, and very indistinctly separated ~from 
the surrounding tissue. The most common situations are the region 
of the third and fourth ventricles and the aqueduct of Sylvius. 
The gray matter is more often involved than the white. 

Etiology. — The cause is probably in all cases the presence of 
infection in the body, such as influenza, typhoid fever, or septicemia. 
Authors, whose opinions we must respect, have, however, described 
encephalitis as the result of simple concussion of the brain, or of 
various forms of poisoning, such as lead. The difficulty in the latter 
group of cases is due to the close resemblance between encephalo- 
malacia and encephalitis. Collections of round cells, with slight 
degenerative changes in the nervous system, have been described 
in chorea, and have been supposed to represent the subacute or 
chronic form of encephalitis. The observations are, however, at 
present insufficient to establish this point. References will be 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 777 



made again to it under the heading of Chronic Encephalitis. Some 
years ago, various observers reported the occurrence of acute 
encephalitis in new-born children, but it has since been shown 
that compound granular cells occur normally in the brain of the 
fetus and persist for some days after birth. 

Pathologic Anatomy. — The two most important changes are 
those in the color and consistency. The former is usually slightly 
darker than normal, but may, if, as is not unfrequently the case, 
extensive hemorrhage has occurred, become a bright red, resem- 
bling, upon inspection, an area of hemorrhage, or perhaps more 
closely, an area of red softening. The consistency is always 
decreased, probably as a result of serous infiltration. Often the 
diseased area projects slightly from the surface of the section. 
Microscopically the characteristic change is the perivascular 
round-cell infiltration. This usually involves the majority of 
vessels in the lesion, and may also be found in regions of the 
brain in which softening has not already commenced. Usually 
there is the characteristic inflammatory congestion, the blood-ves- 
sels, and particularly the small capillaries, being sometimes greatly 
distended and packed with red blood-cells. In some cases 
thrombi have formed. Hemorrhages are exceedingly frequent ; 
these are sometimes punctiform and sometimes diffuse extrav- 
asations into the tissue. Often they appear to represent rupt- 
ured capillaries, and produce a peculiar speckled appearance on 
the surface of section. In the early stages the cellular exudate 
is chiefly composed of polynuclear leukocytes. If the process is 
more advanced, these may exhibit more or less degenerative 
changes. Later they are replaced by mononuclear cells, probably 
representing proliferation of the endothelial cells, and perhaps of 
the neuroglia-cells. The ganglion-cells in the inflammatory re- 
gion undergo rapid degeneration, usually passing through various 
stages of chromatolysis, until they are reduced to little colorless 
vesicles of irregular form. The nerve-fibers also degenerate ; the 
myelin forms fatty droplets ; the axis-cylinders at first swell and 
then share in the granular disintegration. In the midst of the 
focus, the neuroglia ordinarily shares in the softening. At the 
periphery there is usually a noticeable proliferation of the neu- 
roglia-cells and the formation of a coarse, thick network of neu- 
roglia-fibers. Of course, these changes are not found about very 
early lesions. In the earliest stages compound granule-cells are 
usually absent ; later they may appear in considerable numbers, 
but their presence is by no means sufficient to indicate the existence 
of an acute or chronic inflammatory process. Disappearance of 
the tangential fibers in the cortex, in lesions situated in this area, 
have also been described. Ordinarily in these forms of encepha- 
litis, the rest of the brain exhibits no macroscopic changes, and 
often none can be detected by the microscope. The membranes 



778 



TEXT-BOOK OF PATHOLOGY. 



are smooth, the vessels of normal elasticity, and not surrounded 
by a round-cell infiltration. Complete resolution may perhaps 
occur ; of course, this can only be supposed from the clinical 
symptoms of the disease, there being no definite experimental or 
pathologic evidence to support it. 

The focal lesions may undergo softening and lead ultimately to 
scar-formation ; and if they are extensive, there will be considera- 
ble atrophy of the affected part of the brain. The great majority 
of cases, however, in all probability terminate fatally. The nature 
of the process is generally accepted to be primarily vascular ; the 
secondary changes being the result of alteration in the nutrition 
of the surrounding part. 

Suppurative encephalitis has already been in part described in 
connection with purulent meningitis. In that condition, the pyo- 
genic emboli appear to enter the brain-substance along the lym- 
phatics that dip into it from the pia. They are usually small, not 
circumscribed, and more apt to be found in the gray matter of the 
cortex, particularly near the base of the brain and in the struct- 
ures adjacent to the ventricles, than in the white substance. Oc- 
casionally, larger collections, forming rather ill-defined abscesses, 
are found. In a brain that I recently removed at autopsy, the 
changes in the pia-arachnoid were slight and were limited to a 
small area over the motor region for the leg on the left side ; but 
beneath this there was an extensive area of purulent infiltration 
of the brain-substance, not sharply circumscribed. 

Abscess of the brain is a condition characterized by the pres- 
ence in the brain-substance of one or more cavities containing pus. 
The usual cause is suppurative bone-disease, particularly that re- 
sulting from otitis media. The condition may, however, occur in 
general pyemia as a result of metastasis from some neighboring or 
remote focus of suppuration. Suppuration may also occur in the 
course of pneumonia, or in chronic suppurative diseases of the 
lungs, such as fetid bronchitis. Direct infection of the brain, 
either experimentally or as a result of wounds penetrating the 
skull, has also been observed. In many of these cases the nature 
of the transmission is clear ; thus the abscess resulting from dis- 
ease of the ethmoidal sinuses or from direct inoculation is usually 
situated in the immediate neighborhood of the original focus. 
Abscess secondary to pulmonary disease is usually found at the 
base of the cerebral hemispheres, and is probably transmitted 
along the retropharyngeal lymphatics. Abscess due to injury 
without penetration of the skull has occasionally been recorded. 
Sometimes it is found in the contused area, sometimes on the 
opposite side of the brain. The micro-organisms that have been 
found in the pus are practically all the pyogenic forms. The 
most frequent are, perhaps, the staphylococcus, the streptococcus, 
and the pneumococcus. Occasionally the actinomyces, the Bacillus 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 779 



pyocyaneus and the Bacillus tuberculosis have been found, the 
latter in cases that were apparently acute abscesses of the brain, 
and not softened solitary tubercles. 

Statistical studies of the literature show that in about two- 
thirds of all cases the cerebrum is the seat of the lesion. In the 
remaining third it is chiefly the cerebellum. Unusual seats are 
the pons, crura, and medulla. This distribution does not, of 
course, apply to the disseminated forms of purulent encephalitis. 
Solitary abscesses are usually the result of embolism or extension 
from the bones. They may be small or of considerable size, and 
one is on record from which 400 c.c. of pus were removed. They 
may be either surrounded by softened brain-substance or dis- 
tinctly encapsulated. The latter condition usually occurs if they 
have lasted any length of time — that is, three or four weeks ; 
although cases are on record in which a distinct wall did not 
develop about an abscess that had existed for several months. 
The wall, when it exists, varies in thickness from a half to several 
millimeters. The contents of the cavity are pus and detritus, and 
in it may frequently be found thrombosed blood-vessels. The 
surrounding brain-tissue is usually undergoing softening. It may 
be either white, or, as a result of hemorrhagic extravasation, red 
in color. The abscesses usually spread more or less gradually ; 
that is to say, there is probably no tendency to heal spontaneously. 
If large, they cause considerable intracranial pressure, which is 
indicated by the flattening of the convolutions or bulging of the 
brain after the skull has been trephined. Those due to punctured 
wounds are usually associated with meningitis. Those due to 
caries must also be associated with inflammatory changes in the 
meninges, and not unfrequently there is thrombosis of the cerebral 
sinuses. Microscopically, we find the ordinary characteristics of 
pus. The wall or periphery is usually undergoing fatty degener- 
ation, and there is a considerable accumulation of round cells in 
the surrounding tissue. Multiple abscesses are usually metastatic. 
A group may be found either in one situation in the brain or they 
may be very widely distributed. Occasionally the course of the 
case is so chronic that secondary degeneration may occur. In 
such a case, examined by Sailer, with abscesses in the cerebellum, 
cerebrum, and particularly the pons, there was degeneration of 
both pyramidal tracts. This, of course, is a rare condition. 
In cases of severe encephalitis, more or less pronounced changes 
may be observed in the ganglion-cells in other parts of the cen- 
tral nervous system. 

Primary Acute Hemorrhagic Encephalitis. — Strumpell has de- 
scribed under this name a form in which the dura was normal but 
somewhat dry ; the pia injected, the centrum ovale softened, ede- 
matous, slightly pinkish or gray, and marked by fine hemorrhagic 
points. Microscopically there were no granular cells, but drops of 



780 



TEXT-BOOK OF PATHOLOGY. 



myelin and some detritus. There was some hyperemia and cel- 
lular infiltration of the pia. The ganglion-cells of the cortex were 
normal. In the white matter the vessels were distended with 
blood and surrounded by thick masses of round cells ; the peri- 
vascular spaces were distended ; the neurogliar tissue coarser than 
normal. In many situations there was bleeding from the capil- 
laries. 

General Progressive Paralysis. — There has been much 
diversity of opinion concerning the true nature of general pro- 
gressive paralysis. The lesions hitherto described have varied in 
nature and situation. Nevertheless, there seems to be good reason 
to accept an infectious origin of the disease, and unquestionably 
the symptomatology and, to a certain extent, the morbid changes 
indicate that the brain is the organ chiefly involved. The changes 
found most frequently are as follows : the dura mater is adherent to 
the skull ; it may be thickened, and often shows upon its under 
surface the exudate of a hemorrhagic pachymeningitis. The 
arachnoid is thickened and opaque, particularly along the course 
of the veins ; and in the subarachnoid space there is often a con- 
siderable effusion of liquid. The pia mater is thickened and 
opaque, and may or may not be adherent to the cortex ; in the 
latter case the subpial areolar tissue is distended with fluid. 
Microscopically, there is often found a round-cell infiltration about 
the blood-vessels ; their walls are thickened and show some 
hyaline degeneration. The fluid in the areolar spaces may be 
clear, or, as is more commonly the case, it is viscid and even colloid 
in nature. The gross appearance of the brain is frequently con- 
siderably altered. The convolutions are flattened ; the sulci 
broader than normal ; the consistency of the brain is slightly in- 
creased ; the cortex is usually pale and greatly reduced in thick- 
ness. The white matter may appear to be slightly looser in text- 
ure, but ordinarily presents no change. Microscopically, the 
blood-vessels in the cortex have thickened walls, and occasionally 
one is found with a completely obliterated lumen. There is 
usually distention of the perivascular spaces, which may be filled 
with round cells and various products of degeneration, such as 
pigment-granules. The glia-cells are greatly increased in number, 
although it is difficult to decide whether this is absolute or relative. 
The neuroglia-fibers are usually slightly coarser than normal. The 
tangential fibers of the cortex may be reduced in number or 
entirely absent. The ganglion-cells exhibit a great variety of 
alterations. The protoplasmic processes are varicose, and when suf- 
ficiently well impregnated show the absence of the gemmules. 
The axis-cylinder is usually distinct, due to the degeneration of 
the myelin-sheath. The body of the cell may be irregular and 
vacuolated, and there is often extensive chromatolysis. The ventri- 
cles of the brain are usually slightly distended, probably the result 



DISEASES OF THE BRATN AND ITS MEMBRANES. 781 



of simple atrophy, and the choroid plexus is often cystic. Changes 
are frequently found in the spinal cord. The ganglion-cells in all 
parts show pronounced degenerative characteristics. This is par- 
ticularly interesting in view of the fact that the motor symptoms 
progress so gradually. The posterior roots are often slightly 
degenerated, and there is systemic degeneration of the posterior 
columns not unlike that found in the early stages of tabes dor- 
salis, excepting that ordinarily it is most pronounced in the cervi- 
cal region. The pia and arachnoid of the cord, particularly those 
portions covering the posterior columns, are thickened and more 
or less adherent. The dura is often markedly thickened, and may 
exhibit pachymeningitis. The etiology of progressive general 
paralysis is not clear. The great majority of cases commence in 
middle adult life, and have been preceded by an attack of syphilis. 
Certain cases, however, fail to give any syphilitic history, and pre- 
sent no signs of the disease. 

Chronic encephalitis may take the form of sclerosis or of 
scar-formation, which is really but a variety of sclerosis. 

Lobar sclerosis is usually an extensive but sharply circum- 
scribed process affecting the whole or part of one or more lobes of 
the brain. The involved area is usually considerably diminished 
in size. The convolutions are smaller, the sulci broader, but, of 
course, not so deep ; the surface is often finely granular, and the 
pia is adherent. The consistency is greatly increased, the tissue 
being almost like cartilage. Microscopically there are the same 
changes found in the other forms — that is, excessive proliferation 
of the neuroglia, with partial or complete disappearance of the 
nervous elements. The cause appears to be some vascular dis- 
turbance occurring during fetal existence, as the localization nearly 
always corresponds to the distribution of one of the arteries sup- 
plying the brain. If the anterior cerebral artery is affected, the 
frontal lobe is sclerotic. If the artery of the Sylvian fissure is 
involved, there will be sclerosis of all the hemispheres, with the 
exception of a part of the occipital lobe ; and if the lesion is situ- 
ated on the proximal side of the lenticular striate artery, this part 
will also be degenerated. If the posterior cerebral artery is oc- 
cluded, the lesion will be found at the tip and in the lower half 
of the occipital lobe. Extensive secondary degeneration always 
occurs in this form. 

Multiple sclerosis is a condition characterized by the formation 
throughout the nervous system of various foci in which the neu- 
roglia is somewhat hyperplastic, the myelin-sheaths more or less 
degenerated, and the axis-cylinders, as a rule, slightly, if at all, 
affected. The sclerotic areas are of very irregular size and dis- 
tribution, and are much more frequently found in some situa- 
tions than in others. When they affect the white matter of the 
brain and cord they appear as grayish or grayish-pink areas, 



782 



TEXT-BOOK OF PATHOLOGY. 



which may even, if at the surface, be observed through the pia. 
They resemble the gray matter of the cord too closely to be clearly 
distinguished from it. Their edges are usually sharp. After hard- 
ening in Miiller's fluid they appear of a bright-yellow color and 
are exceedingly distinct. The smallest may be only a millimeter 
in diameter, and the largest may occupy the whole transverse sec- 
tion of the spinal cord or even entire convolutions of the brain. 
Occasionally sclerotic areas may be found in the nerve-roots. The 
most important change that is found upon microscopic examina- 
tion is a thickening of the walls of the blood-vessels. This re- 
sembles hyaline degeneration, and may be so extreme that the 
lumen is almost obliterated. The perivascular lymphatic space 
is often filled with cells containing droplets that stain black with 
osmic acid. Occasionally the vessels appear to be increased in 
number, although this is possibly due to contraction of the sur- 
rounding tissue bringing them more closely together. Immedi- 
ately around the diseased vessels the neuroglia is proliferated. 
In the center of the foci the neuroglia-cells are not markedly 
increased ; in the periphery, however, they seem to have under- 
gone a distinct hyperplasia. The neuroglia-fibers throughout are 
somewhat thicker and more irregular, and form a large-meshed net- 
work. In the midst of the neuroglia compound granular cells 
and amyloid bodies are often found. If stained by Weigert's 
method, it is at once evident that the myelin-sheaths have disap- 
peared almost entirely, all the sclerotic areas appearing bright 
yellow. If the Marchi method be used, however, a certain 
number of degenerated myelin-sheaths will be found, as a rule, 
still present. The edge of the sclerotic area does not end as 
sharply as appears macroscopically, but gradually fades into the 
healthy tissue. The axis-cylinders, in spite of the destruction of 
the myelin-sheaths, are nearly always present, and apparently 
normal, a fact which explains the absence of secondary degenera- 
tion beyond the lesions. In those situations where the hyperplasia 
of the neuroglia-fibers is most pronounced, the axis-cylinders may 
be swollen or show partial fatty degeneration, or be entirely ab- 
sent. PopofF believes that these persistent axis-cylinders are not 
those that originally pass through the lesion, but are regenerated 
nerve-fibers ; a view, however, for which there is not sufficient 
proof. The ganglion-cells are shrunken and pigmented, and may, 
in rare cases, completely disappear. In advanced cases of the dis- 
ease, the process resembles more closely a chronic myelitis ; the 
axis-cylinders passing through the lesion may be totally destroyed 
and secondary degeneration occur. In those cases that have been 
studied in the early stages of the process perivascular inflamma- 
tory changes have been present, and it is about these that the scle- 
rotic areas have formed. In some cases thrombi have been also 
detected in the vessels, and many of them showed the early stages 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 783 



of hyaline degeneration. For this reason, and beeause dissemi- 
nated sclerosis frequently develops after an infectious disease, it is 
generally accepted that the process is due to infectious embolism, 
a view particularly supported by Marie. Certain authors, how- 
ever, particularly Taylor, hold that the vessels are not the primary 
origin of the disease, as in many of the sclerotic foci they are 
perfectly healthy. 

INJURIES TO THE CENTRAL NERVOUS SYSTEM. 

Injuries to the central nervous system produce a great 
variety of lesions, according to their nature and severity. 

Concussion, either from a single shock or from repeated blows, 
may give rise to transient or permanent changes. Ordinarily 
there is considerable hemorrhage at the site of the blow. This 
may be either between the dura and the skull or between the 
arachnoid and the pia. Not infrequently, hemorrhage is also found 
in the subarachnoid space of the opposite side (hemorrhage by 
contre coup). This is explained either by supposing a flattening of 
the elastic skull or by ascribing it to the force with which the 
brain rebounds against that side. Small hemorrhages are not in- 
frequently found in the central nervous substance, and appear to 
occur particularly in the direct line of the force applied to the 
skull. In the latter case autopsies have shown the existence some- 
times of multiple hemorrhages, sometimes of disseminated areas 
of sclerosis in the white and the gray substances. Occasionally 
in the spinal cord, after experimental repeated concussions, 
changes, somewhat systemic in character and affecting chiefly 
the posterior columns, have been observed. The hemorrhages 
may be punctate or, in some cases, particularly if the injury is 
severe and the arteries are diseased, massive. 

Lacerated wounds of the brain are usually produced by fract- 
ure of the skull. There is extensive interstitial hemorrhage 
and softening, and the surrounding tissue is edematous. If only 
subdural hemorrhage occurs, it may produce compression with 
secondary yellow softening. Any of these lesions may heal with 
the formation of a scar and the production of more or less exten- 
sive secondary degeneration. Extensive lacerations of the brain 
are sometimes the result of injury during birth, giving rise to so- 
called cerebral palsies of childhood. In these cases, as the central 
nervous system is not fully developed when the injury occurs, there 
is hypoplasia of the affected parts. 

Punctate wounds of the brain are due to fragments of bone, to 
sharp instruments, or to bullets. In nearly all cases a certain 
amount of infection occurs, giving rise to encephalitis. The in- 
jured area usually undergoes complete necrosis, and this extends 
for some distance into the surrounding tissues. The necrotic area 



784 



TEXT-BOOK OF PATHOLOGY. 



is composed of a granular detritus, in the midst of which are 
found altered blood-pigment and broken-down nuclei. At the 
periphery there is usually some granulation-tissue, proliferation 
of the neuroglia, and more or less round-cell infiltration, accord- 
ing to the intensity of the inflammatory process. Experimental 
lesions may be produced in various ways ; the most interesting 
results, perhaps, being those found after the introduction of for- 
eign bodies, or after careful aseptic laceration. In either case, 
shortly after the operation, necrotic changes will be found in the 
enlarged area. There is marked proliferation of the neuroglia- 
cells, even as early as the third day, and of the neuroglia-fibers. 
New capillaries may be seen pushing into the area, the endothelial 
cells of their walls exhibiting karyokinetic figures. The nervous 
tissue in the immediate neighborhood is in various stages of de- 
generation. The myelin-sheaths form balls of fat ; the ganglion- 
cells become swollen, vacuolated, and lose their protoplasmic proc- 
esses. If there has been much hemorrhage, the blood-pigment 
will be found in irregular homogeneous masses or in the form of 
hematoidin-crystals. Later, evidences of regeneration in the nerv- 
ous tissue may be observed, particularly the appearance of karyo- 
kinetic figures in the nuclei of the ganglion-cells. The enlarged 
area is ultimately replaced by a mass of coarse neuroglia-fibers 
containing, usually, fewer cells than normal. That true regen- 
eration of the central nervous system ever occurs in the human 
body is exceedingly doubtful ; indeed, it is not certain that it occurs 
in any of the vertebrates, although after removal of the tail in liz- 
ards a spongy mass of neuroglia may be found in the new organ. 

INFECTIOUS DISEASES. 

Tuberculosis occurs in the brain in the form of miliary tu- 
bercles or as large masses, the so-called solitary tubercle, or tyroma. 

Miliary tubercles are met with in association with tuberculous 
meningitis. They are most frequent at the base of the brain. 

Solitary tubercles occur independently of tuberculosis of the 
meninges. They are more frequent in children than in adults, 
and usually occur in cases in which there is tuberculosis of other 
parts of the body, notably the lymphatic glands. The infection 
reaches the brain through the blood-vessels. The lesions are 
rounded masses of grayish or yellowish color, sometimes showing 
fresh gray tubercles at the periphery. The growth of the mass is 
caused by increase in size of the original tubercles and by con- 
glomeration of new-formed tubercles at the periphery. Early 
caseation is usual. Secondary infection of the pia sometimes occurs. 

Syphilis appears in the brain in the form of gummata or as a 
diffuse vascular disease with secondary degenerative conditions. 

Gummata usually begin in the subarachnoid space, originating 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 785 



in the membranes and involving the brain-substance secondarily. 
The dura may be simultaneously involved, and the three mem- 
branes may be adherent to each other and firmly attached to the 
brain. Primary gumma of the brain-substance is certainly very 
rare. In the earlier stages the gumma is a grayish and rather 
translucent growth, but secondary caseation occurs so rapidly that 
the primary stage is rarely observed. As a rule, the lesion appears 
in the form of an irregular, dry, caseous area occupying the cortical 
portion of the brain and attached to the pia and arachnoid, and 
even the dura. Microscopically the substance of the growth con- 
sists of round and spindle or stellate cells in the earlier stages, 
and of granular material in the later stages. The cerebral sub- 
stance surrounding the growth is more or less softened and degen- 
erated. The blood-vessels in the affected area or its vicinity are 
the seat of endarteritis, which in some cases causes complete occlu- 
sion of the lumen. In hereditary syphilis symmetric gummata of 
the brain are occasionally found. 

Syphilitic disease of the blood-vessels of the brain takes the 
form of more or less diffuse endarteritis. Secondary degenerations 
and softening, or sclerosis, of a diffuse or focal character, may re- 
sult from the vascular disease ; but neither these changes nor the 
vascular changes are peculiar and distinctive. 

Actinomycosis of the brain is generally secondary to actino- 
mycosis of the tissues of the neck, and results from extension up- 
ward through the base of the skull. The membranes are first in- 
volved ; the brain-substance secondarily. The lesion may take 
the form of a chronic abscess or may be tumor-like in appearance 

TUMORS. 

Tumors of the brain are important clinically on account 
of their situation rather than on account of their nature. The 
most common is probably glioma, but almost equally as com- 
mon is sarcoma. Carcinoma, excepting the form springing from 
the lateral ventricles, is almost never a primary growth, but 
secondary nodules are frequently found in the brain. Cho- 
lesteatoma, lipoma, endothelioma, and teratoid cysts also oc- 
cur, but they spring from the membranes, and have been de- 
scribed in connection with them. Gumma and tyroma also 
occur very frequently in the brain, but as their etiology is in- 
fectious they are described in connection with the infectious 
conditions. 

Glioma usually appears as an infiltrating mass, causing little 
alteration in the structure of the brain, somewhat harder in con- 
sistency than the brain-substance, and slightly darker. It is 
rarely a multiple growth, and shows no marked predilection for 
any particular portion of the brain, although it occurs more fre- 

50 



786 



TEXT-BOOK OF PATHOLOGY. 



quently in the cerebral hemispheres than in the basal ganglia or 
the cerebellum. It always springs from the neuroglias tissue of 
the central nervous system, and is remarkable for its extreme 
richness in cells, that by suitable staining-methods may be shown 
to possess protoplasmic processes (astrocytes). These protoplasmic 
processes, either wholly or in part, form the so-called matrix of 
the tumor, which appears to be composed of numerous fine, inter- 
lacing fibers, in the midst of which, by the ordinary staining-methods, 
the cell appears to lie. Usually the tumor is exceedingly vascular, 
the vessels consisting of small capillaries or larger spaces lined 
with endothelium, and this vascularization may be so excessive 
that the tumor in parts has a delicate pinkish or reddish color, giv- 
ing to the cross-section a mottled appearance. Stroebe considers 
as one of the characteristics of this tumor the fact that it does not 
infiltrate the pia mater, and can invariably be shown not to spring 
from it. In some cases the consistency of the tumor is quite hard, 
and in these the cellular elements are increased in amount propor- 
tionately to the fibrous tissue. Ordinarily true nervous tissue is 
absent from the midst of the tumor, the mass in the center being 
made up of the neuroglia-tissue. This gradually diminishes to- 
ward the periphery, and ultimately fades into the true nervous 
tissue, that may be somewhat edematous. In some cases, however, 
as in ordinary sclerosis of the central nervous system, myelinated 
nerve-fibers may be found in the midst of the tumor, and it fre- 
quently happens that the secondary degeneration extending from a 
glioma is much slighter than the apparent extent of the process 
would lead one to expect. Occasionally, either glioma-cells, or 
possibly ganglion-cells, that have undergone proliferative changes 
in the midst of the growth, may be found. These are much larger 
than the ordinary cells and contain numerous branched processes, 
and often one or several large nuclei. This is the so-called gan- 
glionar neuroglioma. 

Some pathologists hold that the starting-point of glioma is always one 
or more ependymal cells that have been displaced in embryonal existence 
and have failed to assume the type of glia-cells, basing their theory in part 
upon the atypical shape of many of the glioma-cells. 

Sarcoma of the brain is probably the next most frequent 
tumor. It usually occurs in middle adult life, although it is quite 
frequent in children. The commonest seat is the cortex, which it 
probably invades from a primary focus of proliferation in the 
membranes. The tumors are ordinarily nodular growths, usually 
distinctly circumscribed from the surrounding tissue, and in some 
cases even surrounded by a fibrous capsule, from which they can 
be readily removed. They are rather firmer than the brain-tissue, 
and sometimes slightly umbilicated if at the surface. The surface 
of section is pale and dry, but frequently mottled on account of the 
presence of hemorrhages. If primary, the sarcomata are single ; if 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 787 



secondary, more frequently multiple, and in these cases they are 
very apt to be found upon the convex surface of the hemispheres, 
forming, if large, irregular flattened masses. Histologically, almost 
any type of sarcoma may be found, the most frequent, perhaps, 
being the round-cell, non-pigmented form. Giant-cells are very 
frequently found. In the midst of true sarcoma, proliferated 
fibrous tissue is not found, but many of the tumors are traversed 
by fibrous trabecule, and some of them contain considerable 
masses of fibrous tissue, giving rise to the so-called fibrosarcoma. 
Ordinarily the tumors are extremely vascular, and occasionally 
contain interstitial hemorrhages. The surrounding brain-tissue 
shows the symptoms of marked compression, is edematous, and 
may contain small interstitial hemorrhages. The true nervous 
substance is ordinarily degenerated, and we find extensive second- 
ary degeneration as a result of the presence of the tumor. Sar- 
coma springs primarily from the brain, and nearly always grows 
toward the surface and infiltrates the pia mater. 

Certain forms of tumors have been described that appear to 
spring from the adventitia of the blood-vessels. They consist of 
masses of cells usually sharply circumscribed, somewhat cylindri- 
cal in shape, having in their center a small lumen in which blood- 
cells may sometimes be detected. These are the so-called peri- 
thelioma. 

Many authors believe that a combination of glioma and sarcoma may- 
occur, and gliosarcomata have been frequently described. As the neuroglia- 
tissue has the functions of connective tissue, and in many respects resembles 
it in its pathologic processes, it is natural that a glioma should be similar 
to a sarcoma, and this has possibly caused an error of diagnosis in some 
cases. As the two tumors arise from tissue of different natures, and develop 
in different situations, their combination is theoretically unlikely. 

Fibroma occurs as a hard, circumscribed tumor, sometimes 
found in the hemispheres, but it is extremely rare. 

lymphangioma appears to arise from the pia. 

Osteoma is usually an extension inward from the skull or 
membranes, but occasionally occurs as a tumor, apparently origi- 
nating in the brain-substance, forming hard masses from the size 
of a pea to that of a cherry, and somewhat irregular in shape. 

Psammoma. — This special term has been given to tumors 
containing calcareous granules. It has already been mentioned in 
connection with the choroid plexus and the membranes. Occa- 
sionally circumscribed fibrous tumors containing calcareous gran- 
ules are found in the brain- sub stance, but these are extremely 
rare (Fig. 352). 

Carcinoma of the substance of the brain is invariably a 
metastatic growth. It appears either as small, round, circum- 
scribed nodules, of firm consistency and pale color ; or as larger, 
more or less infiltrating masses with softened interior. Histologi- 
cally, the tumor may present any type of carcinoma, according to 



788 



TEXT-BOOK OF PATHOLOGY. 



the nature of the primary growth. It usually replaces entirely 
the nervous tissue, either pushing it aside or destroying it, and 
gives rise, therefore, to more or less pronounced secondary degen- 
eration. Multiple metastatic carcinomatous growths, however, 
may exist in the brain without causing clinical symptoms. 

THE CHOROID PLEXUS. 

The choroid plexus, as has been stated, consists of a plexus 
of vessels derived from the mesoblast, that are everywhere cov- 




Fig. 352.— Psarnmoma, showing calcareous spicules and whorls. 



ered by a layer of cuboidal or columnar epithelium. Histologi- 
cally, therefore, it consists of an inner layer of endothelial cells 
and an outer layer of epithelial cells, separated by a small amount 
of areolar fibrous tissue. This condition is most distinct and 
typical in the lower vertebrates, particularly in amphibians, in 
which the choroid plexus consists, in some parts, of a single 
vessel covered by epithelial cells. The structure of the choroid 
plexus, therefore, bears a very close resemblance to the structure 
of the glomeruli of the kidneys, and, as it is obvious that the 
blood-vessels of which it is composed can have no nutritive func- 
tion, excepting in so far as they supply the epithelium that covers 
them, it has been supposed that the choroid plexus is a secretory 
organ, its object being to secrete the cerebrospinal fluid. This 
theory is sustained by the fact that the cerebrospinal fluid differs 
in composition from the lymph, or from the fluid poured out in 
serous exudations. It would naturally be supposed, therefore, 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 789 



that in all conditions in which the alterations in the composition 
of the cerebrospinal fluid have been detected, there is primarily 
some disease of the plexus. 

Hypersecretion. — In certain cases in which communication be- 
tween the cavities of the brain and the interior exists — as, for 
example, through the ethmoid plate of the nose — there is distinct 
hypersecretion of the cerebrospinal fluid. In a case described by 
St. Clair Thomson, as much as a pint was discharged in twenty- 
four hours. In these cases, if for any reason the flow is 
checked, symptoms of intracranial pressure occur. Regarding 
the pathologic changes in the choroid plexus that are associated 
with this condition we have at present no information. Hy- 
persecretion probably also takes place in all inflammatory con- 
ditions. 

Inflammation. — In inflammatory conditions, particularly men- 
ingitis, encephalomyelitis, and ependymitis, either separate or com- 
bined, and associated with the presence of an abnormal quantity 
of albumin in the cerebrospinal fluid, more or less inflammation 
of the choroid plexus is usually found. This is indicated particu- 
larly by round-cell infiltration about the vessels and beneath the 
epithelium. Sometimes there is a slight amount of exudation 
upon the epithelial surface, and occasionally small foci of suppura- 
tion can be detected. 

Infectious Diseases. — Among the infectious diseases the only 
one of importance is tuberculosis. In this condition miliary 
tubercles or large cheesy foci may be found. 

Chronic inflammation appears to be exceedingly rare, or, what is 
probably more accurate, has rarely been described, for there is 
every reason to believe that the choroid plexus shares in all con- 
ditions that involve the pia mater. Atheromatous conditions seem 
to be very infrequent, but a certain amount of thickening of the 
walls of the vessels may be obseryed in old age. A certain 
amount of overgrowth of connective tissue, sometimes associated 
with slight round-cell infiltration, is also occasionally found in old 
people. 

Hemorrhage may take place into the choroid plexus, and is 
usually an agonal phenomenon. 

Degenerations. — Calcification is the most frequent of the infil- 
trations. This may be recognized by the gritty sensation upon 
cutting into the choroid plexus. Microscopically, the calcareous 
nodules appear as minute dark granules that stain purplish with 
hematoxylin. Masses of cholesterin are by no means uncommon ; 
they rarely present the form of typical cholesterin-plates, but are 
somewhat irregular in outline, of a faint yellowish color, and shine 
brightly when examined by oblique light. Both conditions are 
common in old people. 



790 



TEXT-BOOK OF PATHOLOGY. 



Pigmentary infiltration probably also occurs, certainly in mala- 
ria, and perhaps in old age. 

Amyloid degeneration occurs in cases of amyloid disease. 

Tumors. — A great variety of tumors occur in the plexus. 
Cysts may be either retention- or extravasation-cysts, or parasitic. 
The retention-cysts may be lined with epithelium, and probably 
represent adhesions at the edges of fissures with persistence of 
secretory activity. More commonly they are lined with endothe- 
lium and represent dilated lymph-spaces. They may be single or 
multiple, and often are more numerous upon one side of the brain 
than on the other. They appear as small translucent sacs, filled 
with a clear, slightly yellowish liquid, or else a colloid-like, viscid 
mass. Parasitic cysts are usually due to Taenia solium. They 
may be either single, the Cysticercus cellulosse, which may be 
attached to the plexus or lie free in the ventricular cavity, or 
multiple, forming the so-called Cysticercus racemosa of the brain. 

Among the benign tumors, fibromata, possibly but organized 
thrombi, and lipomata have been described. The latter is ex- 
ceedingly rare, and is usually associated with multiple lipomata in 
other parts of the brain. A dermoid cyst has been reported by 
Lebert. Endotheliomata may spring from the lymphatic space. 
They are small, white, infiltrating growths, of firm consistency. 
They possess, microscopically, the ordinary alveolar structure, the 
cavities being lined by endothelial cells, which have proliferated 
and may lie loose in or fill up the lumen. Degenerative changes 
in the stroma or in the cells themselves, particularly of a hyaloid 
nature, are very common in these tumors. Epitheliomata may arise 
from the epithelial covering. Two varieties have been described : 
the papillomatous epithelioma is a small, often microscopic, tumor 
that appears as a villous outgrowth upon the surface of the plexus, 
and is composed of flat or polygonal epithelial cells, with dis- 
tinct evidence of proliferation that may, in the lower layers, cause 
a breaking through of the basement-membrane. These tumors, 
however, are apparently non-malignant. The so-called cylindrical 
carcinomata also occur. These grow very rapidly and usually 
become attached to the wall of the ventricle, and from this situa- 
tion invade the substance of the brain. They are alveolar in 
structure and soft in consistency. There is some doubt as to 
whether these tumors do not arise from the ependyma, and it has 
also been suggested that they are sarcomatous in nature and spring 
from the adventitia of the blood-vessels. They are usually single 
growths and do not give metastases. The choroid plexus, as a 
whole, may be altered, by the presence of cysts, into a mulberry- 
like mass, or by a general fibrous change, into a pale, solid body 
of cylindrical shape with a finely granular surface. 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 791 



THE VENTRICLES. 

The cerebrospinal fluid is a clear liquid with a specific 
gravity of about 1008, a slightly alkaline reaction, and a faint salty 
taste. The fluid obtained from a calf was carefully studied by 
Nawratzki, and it was found to contain 1.093 per cent, of solid 
material, of which about 0.8 per cent, was organic. The average 
quantity of albumin was 0.02 per cent., just sufficient to cause a 
slight opalescence upon boiling. The same author has also ex- 
amined the cerebrospinal fluid in human beings, and finds that it 
is very similar in composition, with the exception of the greater 
proportion of albumin, which at times reaches 0.177 per cent. 
Fresh cerebrospinal fluid from either man or the lower animals 
contains a small proportion of grape-sugar, equivalent to between 
0.17 and 0.27 per cent. According to Halliburton and Hammer- 
sten, the reducing substance is not sugar, but brenzeateehin. This 
reducing substance invariably disappears within a few hours after 
death. 

Pathologically the fluid may show the following changes. The 
color may become yellowish from the admixture of blood, or turbid 
from the admixture of pus. Micro-organisms are frequently found 
in it in all forms of meningitis, but particularly in epidemic cerebro- 
spinal meningitis. It must not be forgotten, however, that in the 
late stages of this and in the early stages of meningitis due to the 
tubercle-bacillus, the fluid may be clear. INawratzki observed a 
considerable increase in the amount of albumin as the only change 
in a case of hemorrhagic pachymeningitis. Microscopic exam- 
ination, even in normal cerebrospinal fluid, usually shows the 
existence of some blood-discs and leukocytes. In pathologic 
changes a greater or less number of pus-cells may be present, 
and often there is a considerable amount of fibrin. 

Hydrocephalus. — Excess in quantity of the cerebrospinal 
fluid in the ventricles is known as hydrocephalus. This may be 
produced by a great variety of causes. It may be congenital, and 
perhaps due to a malformation, but is more often a result of dis- 
ease. Congenital hydrocephalus frequently appears to be due to 
some defect on the part of the parent, and is particularly common 
in the children of drunkards. 

Congenital hydrocephalus internus is characterized by a gradual 
accumulation of cerebrospinal fluid in the lateral and third ven- 
tricles of the brain, probably the result of excessive secretion 
from the choroid plexus (Fig. 353). As a general rule, the fourth 
ventricle is not involved. The aqueduct of Sylvius, however, 
is often dilated. Sometimes the fifth ventricle is distended, or 
the septum has atrophied and disappeared, allowing free commu- 
nication between the two lateral ventricles. Less frequently, the 
infundibulum is distended and forms a small sac at the base of 



792 



TEXT-BOOK OF PATHOLOGY. 



the brain. Usually the disease is manifest at the time of birth, 
and the head may even at this period have attained the circum- 
ference of more than 50 cm. Externally, the head is spherical 
and large ; the face is small, and, with the bulging forehead, gives 
to these patients a characteristic expression. The cranial bones 

are usually more or less separated ; fre- 
quently the edges of the sutures are an 
inch or more apart. The anterior fon- 
tanelle is large and usually bulging. If 
the bones of such a skull be examined, 
it will usually be found that they are 
very thin, and that ossification is in- 
complete. The dura mater is tense, 
and beneath it may be found the 
greatly flattened convolutions. The 
brain-substance seems softer; often 
there is distinct fluctuation, although 
the brain collapses as soon as it is re- 
moved from the cranial cavity. The 
distance from the wall of the ventricle 
to the surface is much less than nor- 
mal, this atrophy seeming to affect the 
white substance more than in the cor- 
tex. The total weight of the brain, 
however, is often normal or nearly so, 
and it is impossible to say that an act- 
ual atrophy has really taken place. 
The substance of the brain is pale, 
probably as a result of the pressure, 
and often softened, particularly in the 
neighborhood of the ventricles, al- 
though this is probably only an unusually rapid post-mortem 
change. The floor of the ventricles may be smooth or slightly 
roughened, and occasionally distinct nodules may be observed. 
In the latter case there is usually considerable proliferation of 
the neuroglia in the cortex, and just beneath the floor of the 
ventricle a sort of sclerosis of the brain-substance. The cere- 
brospinal fluid is usually clear, and not abnormal in consistency. 
Occasionally, however, it is somewhat turbid, particularly if 
there are any signs of old inflammatory action. The choroid 
plexus is often somewhat enlarged, pale, and may contain cysts. 
As the patients increase in age there is usually considerable 
increase in size of the head ; nevertheless, the convolutions grad- 
ually become more rounded, and the white substance appears to 
undergo a sort of redevelopment, for the layer of brain-tissue be- 
tween the ventricle and the surface becomes thicker. Systemic 
degenerations of the white fibers are uncommon. There may, 




Fig. 353.— Congenital internal 
hydrocephalus, with marked 
atrophy of the white substance 
(from Bollinger). 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 793 



however, be marked thinning of the corpus callosum and the ante- 
rior commissure. Cases have been described in which a descending 
degeneration along the pyramidal columns was found in the cord. 

Partial hydrocephalus has been described. It is probably, in 
the great majority of cases, of congenital origin. It may affect 
only one ventricle, or even only a part of a ventricle, as, for ex- 
ample, the anterior or posterior horn of one of the lateral ventri- 
cles. It appears to be the result of an obliteration of one of the 
normal passages by which the ventricles communicate with one 
another. 

External hydrocephalus is the accumulation of fluid that oc- 
curs in the subarachnoid space to replace brain-tissue that has un- 
dergone atrophy, or to fill the cavity of porencephaly. Occasionally 
symmetrical collections of liquid are found, as in a brain that I 
removed from an idiot, in which both temporosphenoidal lobes 
were excavated and replaced by large cysts. 

Acquired hydrocephalus may be either acute or chronic. The 
acute forms are usually secondary to inflammatory changes in the 
meninges, extending to the choroid plexus and to the ependyma, 
or are caused by some abnormal growth pressing upon the veins 
of Galen. In the atrophic brains of the aged dilated ventricles 
are frequently found. 

Acute acquired internal hydrocephalus is usually the result 
of acute basilar meningitis, either inflammatory or tuberculous. 
The brain, in addition to the meningitic changes, presents all the 
characteristics of intense intracranial pressure. The convolutions 
are flattened and pale. The brain-tissue is usually soft, or at least 
softens rapidly after death, particularly the part that surrounds 
the distended ventricles. Upon opening the brain the fluid is 
usually found under considerable pressure, and often almost gelat- 
inous inconsistency. Frequently, microscopic examination of the 
brain-substance will show the presence of acute, disseminated, 
suppurative encephalitis. The ependyma of the ventricles is 
injected and often covered with lymph. In the tubercular form 
it may be roughened, as a result of the presence of numerous 
miliary tubercles. The choroid plexus is injected. In the acute 
forms it also has some lymph upon the surface, and in the tuber- 
cular form may contain miliary tubercles. 

Chronic hydrocephalus is usually a late result of meningitis, 
particularly the epidemic form. Occasionally it is the result of 
gradual compression of the veins of Galen, as, for example, by a 
tumor of the cerebellum. Perhaps most frequently it is the result 
of a chronic granular ependymitis. In these cases the distention 
is more pronounced than in the acute form. The ependyma is 
thickened and opaque, and often contains small hard nodules. 
Occasionally bands of organized fibers may be found in the cavity 
of the ventricle. 



794 



TEXT-BOOK OF PATHOLOGY. 



I£pendymitis may be chronic or acute. The acute form is 
always secondary to meningitis, and is characterized by prolif- 
eration of the ependymal cells and the usual inflammatory changes. 




Fig. 354— Sclerotic nodule in the floor of the lateral ventricle, with wrinkling of the 

ependyma ; X 100 (Sailer). 

Chronic ependymitis is usually associated with sclerosis of the 
brain. The surface is granular or even nodular. The ependyma 




Fig. 355,— Sclerosis of the brain; X 300. 



is thrown into folds, and there is great proliferation of the sub- 
ependymal neurogliar fibers (Figs. 354, 355). 

THE PITUITARY BODY, OR HYPOPHYSIS CEREBRI. 

The hypophysis is a small glandular organ, situated at the base 
of the brain, lying upon the upper surface of the body of the 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 795 



sphenoid bone, and further protected posteriorly by a wall, form- 
ing a cavity which is known as the sella turcica. It varies slightly 
in size, the average weight in the adult being from 0.59 gm. 
(Schonemann) to 0.48 gm. (Comte). It reaches its maximum 
between twenty-one and forty years of age. 

The hypophysis is a double organ, developed from the central nervous 
system and from the alimentary canal. The nervous part originates from 
the middle primary cerebral vesicle as an evagination from the cavity. 
This forms the infundibulum and the small posterior lobe. The larger 
anterior lobe appears to arise from two sources, one, the primitive oral 
tissue in early embryonal life, and the other the anterior portion of the 
alimentary canal ; both portions become contracted at their origins, fuse, 
and are ultimately separated from the alimentary canal, although this 
separation is not complete in some of the lower vertebrata. Histologi- 
cally, the organ may be divided into three parts: the anterior portion of 
the anterior lobe is composed of somewhat polygonal epithelium-cells en- 
closed in alveoli, whose walls are made up of fibrous connective tissue. These 
groups of cells are very irregular, although sometimes they are arranged 
about the periphery of the cavity, leaving in the center a small lumen, 
which, more frequently than not, is rilled with an oxyphilic homogeneous 
mass that is supposed to be colloid. The amount of connective tissue is 
usually relatively small, and it contains a considerable proportion of cells 
as compared with connective tissues of other parts of the body, and is ex- 
ceedingly vascular. The cells are of two kinds, the chromophilic and the 
chromophobic. The former are further divided by Comte into the eosino- 
philic, in which the protoplasm stains deeply and homogeneously with 
eosin, and usually contains vacuoles ; and the cyanophilic cells, in which 
the protoplasm colors dark blue with hematoxylin, and rarely contains 
vacuoles. The protoplasm of the chromophobic cells does not stain. Some 
authors consider that these distinctions are not morphologic, but only indi- 
cate that the different cells are in different stages of secretory activity. 
The posterior part of the anterior lobe usually contains, in man, a small 
bilobed cavity lined with cylindrical ciliated epithelium. In addition, 
there are also a few larger cavities lined by columnar or polygonal epi- 
thelium, and usually filled with colloid material. The posterior or nervous 
lobe consists of neuroglia-tissue, and, according to Berkeley, a few gang] ion- 
cells containing an excess of pigment, and some varicose fibers may be 
found in it. Kolliker, however, denies that there is any nervous tissue at 
all in the posterior lobe, and has been able to find nothing but neuroglia. 

From its analogy in structure to the thyroid gland, it has been 
supposed that the function of the pituitary body is to abstract 
some material from the blood, to alter it, and then to return it to 
the circulation — that is to say, it is one of the internal secretory 
glands. Pronounced changes following its removal or destruction 
cannot, however, be said to have been definitely established. If 
Ave can believe the assertions of those who have systematically 
examined large numbers of these bodies, a normal gland is the 
exception ; thus, Schonemann found only 27 normal specimens in 
110 cases, and Comte 33 in 108. 

Hypertrophy of the hypophysis occurs in cretinism, myx- 
edema, and acromegaly. In some of these cases the hypertrophy 
is due to tumor-formation ; in others, particularly in those occur- 



796 



TEXT-BOOK OF PATHOLOGY. 



ring as a result of removal of the thyroid gland, it appears to be 
compensatory, or rather, as the functions of this gland and the 
thyroid cannot be exactly identical, at least vicarious. This en- 
largement, often apart from tumor-formation, may be very con- 
siderable. De Conlon records a case in which the hypophysis 
weighed 1.55 gm., and, aside from an apparent proliferation of 
the epithelium-cells, was normal in structure. 

Circulatory Disturbances. — The gland, as has been men- 
tioned, is excessively vascular. It is possible that in some cases 
this vascularity may increase and give rise to a true hyperemia, 
although it is difficult to be certain of this. Changes such as 
are found in the thyroid gland in exophthalmic goiter have 
certainly not been described. In case of passive congestion re- 
sulting from thrombosis of the cavernous sinuses intense edema 
may be present. Hemorrhage in the gland is a frequent agonal 
phenomenon. In these cases the blood-cells, usually normal in 
appearance, are found infiltrating the connective-tissue stroma. 
Hemorrhages during life may occasionally occur, and give rise 
to small, deeply pigmented areas of softening, which ultimately 
form scars. 

Inflammation is usually secondary and suppurative. I have 
observed a case in which the anterior lobe was infected from 
the parotid gland, probably as a result of ascending infection 
along the retropharyngeal lymphatics. In this case the capsule 
enclosing the gland was inflamed, and there were small collections 
of round cells in the substance. 

Degenerations. — Infiltrations with either calcareous mate- 
rial or pigment have not been hitherto described. The degenera- 
tions, however, are numerous. The most important and frequent 
is colloid degeneration, the colloid material being found in the 
cavities of the epithelial nests, or even as small masses in the con- 
nective-tissue septa. This may be looked upon as almost physi- 
ologic. It seems to be increased in those conditions in which we 
have reason to suspect increased functional activity of the glands ; 
but also is more pronounced in cases of partial atrophy. Amyloid 
degeneration occurring in the blood-vessels has been observed in 
cases of general amyloid disease. The walls of the blood-vessels 
frequently undergo hyaline degeneration in old age. 

A sort of cheesy or liquefactive necrosis is also observed in the 
center of adenomatous formations, and is probably due to pressure- 
necrosis, as a result of the limited space in which the hypophysis 
is placed. 

Infectious Diseases. — Of the infectious inflammations, the 
only ones of importance are tuberculosis, in the form of miliary 
tubercles, and syphilis, in the form of gummatous nodules. Occa- 
sionally a large single gumma has been observed. 

Tumors are perhaps the most interesting and important 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 797 



changes that occur, and there is still considerable difference of 
opinion regarding their nature. 

Cysts are very common, particularly a form of cystic degenera- 
tion with distention of the follicles by colloid substance. These 
are almost normal in old age, the only interesting feature being the 
atrophy and disappearance of the epithelial cells. Teratoid cysts 
have been described, but are much less frequent than would be 
expected from the complicated embryology of the gland. Of this 
nature is the myoneuroma described by White. 

Of the malignant tumors, the only one hitherto described is 
the sarcoma. This is usually round-cell or spindle-cell in type, 
and apparently springs from the capsule of the gland and replaces 
its substance, but rarely infiltrates the surrounding tissues or gives 
rise to metastasis. Cases have been reported as lymphosarcoma in 
which there were numerous collections of round cells in the alveoli 
of the connective tissue and some hypertrophy of the latter ; appar- 
ently, however, no other lymphatic organs were involved. 

Adenoma of the hypophysis causes increase in the size ; the 
organ remains soft or may be slightly indurated, and is of normal 
color. The resistance of the bony structures that surround it may 
cause the gland to assume extraordinary shapes. Microscopically 
there is proliferation of the epithelium -eel Is, which form long tor- 
tuous and sometimes branched tubes, and often complete atrophy 
of the nervous lobe. These tumors have been described particu- 
larly in connection with the disease known as acromegaly. 

Pathologic Physiology. — The relation of disease of the 
hypophysis to acromegaly is a much disputed question. In all 
cases that have hitherto come to autopsy the hypophysis has been 
found diseased and in all but one, enlarged. In view of the 
analogy of structure between the hypophysis and the thyroid gland, 
and the certain etiologic relation of disease of the latter to myx- 
edema and cretinism, it was at first assumed, almost without ques- 
tion, that acromegaly was caused by disease of the pituitary body. 
Many cases have been reported in which there was disease of this 
gland without any symptoms of acromegaly, and a certain degree 
of general splanchnomegaly has been observed in acromegaly. It 
is, of course, possible that the enlargement of the pituitary is sim- 
ply a part of the latter condition. The thyroid gland, however, 
does not partake of this change, nor do, apparently, any of the 
other secretory organs, the various enlargements being usually the 
result of a hyperplasia of the lymphoid tissue. Neither are the 
changes of other organs as constant as those of the hypophysis. 
There is certainly no characteristic lesion in the latter organ, for 
nearly all forms of disease have been described — adenoma, sar- 
coma, cystic degeneration, and sclerotic change. If acromegaly is 
the result of disturbed function of the thyroid gland, it is probably 
due to excessive rather than deficient functional activity, for, as 



798 



TEXT-BOOK OF PATHOLOGY. 



above stated, the gland is usually enlarged, and pituitary extract 
has proven useless in the treatment of the disease. In the absence 
of definite knowledge of the results of experimental lesions, the 
question must remain at present undecided. 

THE PINEAL GLAND, OR EPIPHYSIS CEREBRI. 

The pineal gland, or epiphysis cerebri, is an outgrowth from the 
roof of the posterior portion of the anterior vesicle of the brain. 
Its base is soon constricted, and it is finally completely separated 
from the primary cerebral vesicle and enclosed in a sheath of con- 
nective tissue which is surrounded by pia mater. Histologically, 
it is found to consist of septa of connective tissue, dividing it into 
numerous alveoli, in which are found epithelial cells, some of 
which are branched. It is very vascular, and contains a plexus 
of sympathetic nerve-fibers. The gland is in all probability 
wholly without function. It really is a hypoplastic or degenerate 
central eye, that is much better developed in some of the reptiles, 
but ceased to exist as a functioning organ in prehistoric times. 

At all ages it contains small calcareous concretions (acervulus, 
brain-sand), which must therefore be looked upon as physiologic. 
It is sometimes enlarged in acromegaly and cretinism, or as a 
result of a hyperplasia of the epithelial structures, giving rise to 
adenomatous or strumous formations. As a result of its position 
it may in these conditions occlude the veins of Galen and produce 
hydrocephalus. Pathologically, aside from the calcareous infiltra- 
tion already mentioned, hyaline degeneration of the blood-vessels 
may occur. There are usually signs of inflammation, more or less 
marked, in cases of meningitis, which may even lead to pus-for- 
mation. Of the tumors, the most important are probably sar- 
comata, springing from the connective-tissue septa. Adenomata 
may also occur. Cystic conditions, associated with the presence of 
hair, cartilage, and other tissues, have been described. 



CHAPTER XIII. 

DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 

THE DURA MATER. 

Diseases External to the Dura Mater. — Among the mi- 
nor processes that may occur externally to the spinal dura mater is 
fatty infiltration, sometimes associated with general obesity, but 
occasionally found in patients that are moderately emaciated. 

Hemorrhage may occur on the external surface of the dura, the 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 799 



blood being found distributed in the extradural areolar tissue. 
The usual cause is traumatism, but it may also occur in convulsive 
conditions. Ordinarily the blood remains circumscribed and forms 
a spinal hematoma ; rarely, a cyst results. 

Diseases of the Dura Itself. — Most of the pathologic proc- 
esses are secondary to some disease of the vertebral column. The 
most important is tuberculosis ; this gives rise to external tubercu- 
lous pachymeningitis, characterized by a collection of cheesy ma- 
terial which may have undergone either softening or necrosis, or 
else contains pus-cells. The dura in the affected region is usually 
considerably thickened, and may have upon its inner surface a 
slight amount of exudate. The character of the lesions is not 
different from that of tuberculosis in other serous membranes 
(Fig. 356). 

Pachymeningitis cervicalis is a localized tuberculosis of the dura 
mater occurring in the cervical region, and characterized by con- 




Fig. 356.— Tuberculous pachymeningitis secondary to spinal caries. 



siderable thickening, sometimes amounting to \ cm. or more. The 
dura is usually adherent to the spinal canal and to the arachnoid 
and pia, the latter showing more or less involvement. The serious 
changes consist of compression of the roots and of the spinal cord, 
the latter especially in the anteroposterior direction. The process 
may extend into the substance of the cord and produce a myelitis 
of the periphery, and occasionally extends deeper and causes more 
or less extensive secondary degenerations. 

Of the acute inflammations the most important is internal 
hemorrhagic pachymeningitis, a process similar to that occurring 
in the dura mater of the brain. It consists of a layer of granula- 
tion-tissue in which many of the capillaries have ruptured, giving 
it a more or less uniform reddish appearance ; it is somewhat 
irregular in outline and of varied extent, and not infrequently 
adhesions form between the dura and the arachnoid. 

Syphilis occurs either in the form of discrete gummata or as a 
regular and diffuse thickening of the inner membrane. 

Tumors from the spinal canal frequently invade the dura. 
The most common of these is sarcoma. This occasions consider- 
able thickening of the dura, and it is often difficult to separate the 
dura from the sarcomatous bone. In consequence of these condi- 
tions there may be pressure and atrophy of the spinal cord. 



800 



TEXT-BOOK OF PATHOLOGY. 



Tumors of the dura itself may be either benign or malignant. 
Of the former, lipomata, which also occur in the brain , are the 
most frequent. Myxomata and fibromata are exceedingly rare. 
Sarcoma may be of the round-cell, angiomatous or alveolar type. 
It is usually irregular in outline, spreading like a fungous mass 
over the surface of the membrane, which exhibits fibrous thicken- 
ing. If small and occurring on the anterior aspect, it may pro- 
duce no symptoms whatever. In this situation it is frequently 
secondary. 

In a few rare instances melanotic sarcoma has been observed. 
Not infrequently a granular sarcomatous mass invades the cauda 
equina and infiltrates it for a considerable distance downward. 
The nerve-roots often fail to show any signs of degeneration, and 
apparently no pressure-symptoms are produced. In some cases 
sarcomata of the dura produce proliferation of the neuroglia-tissue 
in the adjacent portion of the spinal cord. 

Upon the inner surface a variety of tumors have been observed. 
Horsley mentions myxomata, fibromata, carcinomata, and sar- 
comata. In rare cases echinococcus-cysts have been observed, and 
even the cysticercus. 

THE PIA AND ARACHNOID. 

CIRCULATORY DISTURBANCES. 

Active hyperemia precedes and accompanies inflammatory 

changes. It is rarely seen post-mortem, and in the majority of 
cases its existence can only be inferred. 

Passive hyperemia is very common — that is to say, in many 
cases the veins of the pia mater are found to be tortuous and 
greatly distended with blood. This is usually due to post- 
mortem hypostasis. 

DEGENERATIONS. 

Calcareous infiltration sometimes occurs, appearing as 
small, hard plates, rarely more than 0.5 cm. in diameter, scattered 
along the whole length of the spinal cord. It is probably always 
secondary to inflammatory processes, as spinal syphilis and tuber- 
culosis. 

Pigmentary infiltration may occur, but is rare. 

INFLAMMATIONS. 

Acute inflammation, or acute leptomeningitis, is often 
secondary to cerebral meningitis. It may occur, however, inde- 
pendently as a result of local suppurative processes, particularly 
those of the spinal column. It may be serous or purulent in 



DfSEASES OF THE SPINAL CORD AND ITS MEMBRANES. 801 



character, and in the latter an exudate is found upon the inner 
surface of the dura and in the subarachnoid space, often extending 
the entire length of the spinal cord. The microscopic changes 
are essentially similar to those found in the membranes of the 
brain. Involvement of the cord is, however, much more common. 
There is usually extensive round-cell infiltration in the anterior 
commissure and small foci of round cells scattered throughout the 
gray and the white matter, especially in the latter. Frequently 
these can be seen to surround a blood-vessel, but this is not always 
the case, and it is not unlikely that purulent material can enter 
from the lymphatics of the pia. If death does not occur, adhe- 
sions may form between the dura and arachnoid, but these are 
certainly exceedingly uncommon in the cord. 

Chronic leptomeningitis is usually associated with scle- 
rosis of the spinal cord ; thus, in locomotor ataxia the pia mater 
over the posterior column may be opaque and slightly thickened. 
It may also be consecutive to some of the other inflammatory 
processes, and in this form adhesions may be found between the 
dura and arachnoid (pachymeningitis and arachnitis adhesiva). 

In cases of injury of the spinal column, such as fracture, 
caries, etc., in which continuous pressure is produced upon the 
dura mater, it becomes thickened and adherent to the bone and 
may cause pressure upon the spinal cord. In these cases there is 
rarely any round-cell infiltration in the thickened dura, which 
consists almost entirely of fibrous connective tissue and blood- 
vessels ; the latter have greatly thickened walls. 

INFECTIOUS DISEASES. 

Tuberculosis may occur in the form of miliary nodules or as 
small cheesy masses, usually extending a slight distance from the 
pia mater into the substance of the cord. It is disputed whether an 
acute leptomeningitis without miliary or cheesy nodules may be 
caused by this organism alone, but this has not as yet been decis- 
ively established. Solitary tubercles may occur in any part of 
the spinal cord. They are rarely encapsulated. They usually 
consist of an aggregation of round cells with vesicular nuclei, 
and are often softened in the center. 

Syphilis appears as a thickening of the membranes with mul- 
tiple gummata, often projecting into the substance of the cord or 
extending to and involving the dura mater. The vascular changes 
are very characteristic ; nearly all the blood-vessels exhibit the 
typical round-cell infiltration and thickening of the intima which 
have been described in the section on endarteritis syphilitica. There 
are also a perivascular round-cell infiltration and some prolifera- 
tion of the adventitia. The veins may also be involved. The 
lumen of both sets of vessels is usually contracted, and there is a 

51 



802 



TEXT-BOOK OF PATHOLOGY. 



great tendency to the formation of thrombi. In these thrombi 
organization may take place, with the formation of new blood- 
vessels. The spinal cord may also exhibit various lesions, due 
either to pressure or to direct extension inward from the pia. 

In congenital syphilis the upper part of the spinal cord 
appears to be more involved than the lower part, In syphilitic 
leptomeningitis there are often extensive degenerations of the 
tracts in the cord. These involve particularly the lateral and 
posterior columns, giving rise to a combined sclerosis ; and, in 
addition, there is often a narrow band of sclerotic tissue encircling 
the cord and lying immediately beneath the pia. 

ANATOMY OF THE CORD. 

The spinal cord is composed, as are the other parts of the central nervous 
system, of gray and white matter; the gray matter occupying the central 
part, and the white matter being distributed around it. It is of varying size, 
somewhat broader and flatter in the cervical region than elsewhere ; almost 
circular in the dorsal region, and again thicker in the lumbar region. It 
communicates with the rest of the body by means of the spinal nerves, 
which arise anteriorly and posteriorly as roots ; eight from the cervical, 
twelve from the dorsal, five from the lumbar, and five from the sacral re- 
gion. It is surrounded by three membranes: the pia, adherent to it; the 
arachnoid, adherent to the pia, but not dipping into the anterior fissure, 
and the dura mater, which is adherent neither to the arachnoid nor to the 
vertebral column. The gray matter is divided into two parts by the ante- 
rior commissure and posterior septum, each part consisting of an anterior 
horn, a thick, roundish mass, and a posterior horn, a slenderer projection. 
The lateral halves are united by the gray commissure, in which is the central 
canal lined with cuboidal epithelium and continuous with the fourth ventricle 
above. In the anterior cornua are found the large multipolar ganglion- 
cells, whose axis-cylinders pass out through the anterior roots and end in 
the muscles ; commencing in the dorsal region, there is a group of cells in 
the inner portion of the posterior horn, near the gray commissure, which 
are bipolar and whose axis-cylinders pass outward to the cerebellar tract, 
in which they ascend to the vermiform process of the cerebellum. The 
posterior roots are composed of fibers that originate in the spinal ganglia 
and pass into the cord. These spinal ganglion-cells have a single process, 
which careful embryologic investigation has shown to be formed by the fusion 
of two polar processes, that have been brought in contact by the shrinking 
of one side of the cell. This process appears to divide into two fibers, one 
passing outward into the peripheral nerves and usually terminating in the 
sensory corpuscles of the skin, the other passing inward through the poste- 
rior root to the spinal cord. Lenhossek believes that the peripheral fiber 
represents the protoplasmic process of the cell which normally conveys im- 
pulses cellipetally. The white substance of the spinal cord is composed of 
bundles of nerve-fibers that have, for the most part, a common function, a 
common mode of origin and of termination. 

Anatomically the cord may be divided into three regions: anterior, lat- 
eral, and posterior, although these do not correspond to regions embryo- 
logically distinct. According to the manner of development, it should be 
separated into the anterolateral and the posterior regions. 

The most important bundles of fibers in the anterolateral columns are 
those known as the pyramidal tracts, for the reason that they are continu- 
ations of the pyramids of the medulla. They originate in the motor region 
of the cerebral cortex and, in the first cervical segment, decussate through 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 803 



the representatives of the anterior cornua to reach their situation in the 
lateral columns. This decussation does not occur in all of the fibers, many- 
passing down in the direct pyramidal columns and some without decussation 
in the lateral columns. These undecussated fibers subsequently cross to the 
other side through the anterior or white commissure. The fibers of the 
pyramidal columns terminate in arborizations which surround, but are not 
in contact with, the ganglion-cells of the anterior cornua. 

The cerebellar tract has already been described. Anterior to it and close 
to the periphery of the cord is the so-called anterolateral column of Gowers. 
The fibers which form this probably originate in the lateral groups or cells 
in the anterior cornua and in the cells in the middle portion of the spinal 
cord. The column increases in size upward and degenerates in the same 
direction. Its termination is unknown. It also contains fibers that degen- 
erate downward, of whose origin and termination we are ignorant. 

The rest of the anterolateral column is composed of short fibers, uniting 
different segments of the spinal cord. 

The posterior columns are composed of the fibers that enter by the pos- 
terior roots. These fibers divide into two branches, one ascending and the 
other descending, the latter terminating in the gray matter of the posterior 
horn. The ascending fibers may be divided into two groups, the lateral and 
median bundles. The fibers of the lateral bundle are somewhat finer, and 
evidently belong embryologically to a different period, because they acquire 
their myelin-sheaths later. They pass directly into the zone of Lissauer, 
and thence into the substantia gelatinosa of Kolando, and some of them 
terminate in arborizations about the ganglion-cells in the column of Clarke. 
The fibers of the median bundle are coarser. They pass inward, then up- 
ward along the inner side of the posterior horns, and then become the 
column of Bur da ch. The median fibers from the lower part of the cord 
bend inward and continue their course in the column of Goll, terminating 
finally in the nucleus gracilis of the medulla oblongata. The fibers that 
enter the cord in the cervical region pass upward in Burdach's column and 
terminate in the nucleus cuneatus. Other fibers pass forward to the gan- 
glion-cells of the anterior cornua, and have been supposed to be concerned 
in reflex action. Others decussate in the posterior commissure and then 
pass upward in the posterior columns of the opposite side. At somewhat 
regular intervals they give off at right angles fine collateral branches, which 
pass forward, and some of them, at any rate, end in arborizations about the 
cells of the anterior cornua of the gray matter. These are known as the 
reflex collaterals of Kolliker. A small portion of the posterior column just 
back of the gray commissure appears to be composed of fibers uniting the 
different segments. Physiologically, the spinal cord may be ragarded as a 
series of superimposed centers which contain cells sending or receiving im- 
pulses to or from the periphery, and bands of fibers that unite these centers 
with the brain. The functions of these different tracts have already been 
discussed in the Anatomy of the Brain. An important function of the 
spinal cord is the accomplishment of reflexes. These are situated in various 
portions, and according as these portions are intact or involved, the reflexes 
persist or disappear. By means of the distribution of the sensory and 
motor disturbances and the alterations in the reflexes, accurate localization 
of a lesion in the cord is often possible. 

[It is sometimes convenient to identify the nerve-roots in the spinal cord 
for the sake of locating lesions or tracing the alteration in systemic degen- 
erations. The most satisfactory method of doing this is to cut through the 
dura along the anterior and posterior surfaces of the cord. The cord is then 
stretched out at full length and the dura pulled downward as far as the 
roots allow it to go. The root that pierces the dura opposite the conus ter- 
minalis is the second lumbar. The lower cervical roots are all of large 
size. The first dorsal is sometimes smaller, but the difference between it 



804 



TEXT-BOOK OF PATHOLOGY. 



and the second dorsal is still more considerable, and this serves as a check 
upon the previous estimation. Familiarity with the appearance of the cord 
at the different levels also enables one to locate sections with considerable 
accuracy.] 

CONGENITAL ABNORMALITIES. 

Total absence of the cord, or atnyelia, can only exist in 
association with anencephalus. It is interesting to note that the 
spinal ganglia usually persist. Partial absence of the upper 
portion occurs in cases of anencephaly. 

Abnormal smallness is known as micromyelia. The 
cord may be normal in structure, all the elements being propor- 
tionately reduced, but more commonly only certain parts are 
affected, particularly the pyramidal columns, as a result of fetal 
lesions in the motor tract. 

Double cord, or diastematomyelia, is usually localized to 
one portion of the cord, particularly the lumbar region. Occa- 
sionally the cord is completely divided by a bony septum. In 
this case the gray matter in either half presents the normal 
arrangement of the gray matter in the cord. 

Unusual length of the cord may also occur, the conus ter- 
minalis being in these cases elongated and extending to the end 
of the sacrum. 

The spinal roots may be excessive or defective in number on one 
or both sides. This usually occurs in the dorsal region, the com- 
monest condition being the presence of eleven roots on one side. 

The cord may be asymmetrical. This usually involves only 
the pyramidal columns, and is due to incomplete decussation. 

Heterotopia of the gray matter is not infrequent. This may 
consist of doubling of one of the horns ; disorganization of one 
or both horns, or fissures extending into the substance. Accord- 
ing to van Giessen, the majority, if not all, of these cases are the 
result of injury during removal, and are therefore to be regarded 
as artefacts. This statement is, however, too sweeping. Abnor- 
mal bundles, producing heterotopia? and due to alterations in the 
medulla or even higher in the central nervous system, have been 
found. These appearances may also be produced by tumors or 
other conditions causing pressure. 

Dilatation of the Central Canal. — The central canal may 
be dilated, either locally or throughout its whole length. This 
condition is known as hydromyelia, or hydrorrhachus, and is akin 
to hydrocephalus, with which it is sometimes associated. Hemor- 
rhage may take place into these dilated canals and gives rise to 
hematomyelia (vide infra). 

Localized collections of liquid in the subarachnoid spaces are 
sometimes spoken of as hydrorrhachus externa. 

Spina Bifida. — -There may be imperfect closure of the poste- 
rior processes of the vertebrae, giving rise to clefts, which are known 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 805 



as rachischisis. If the membranes of the spinal cord protrude 
through the cleft in an imperfectly closed canal in the form of a 
sac or hernia, the condition is called spina bifida. In some cases the 
skin is still present, and is often covered by an abnormally thick 
growth of hair. In other cases the pia is the only membrane that 
enters into the formation of the wall. It is usually thickened, 
and may be covered with granulations. Sometimes the dilatation 
evidently takes place in the central canal, for the substance of the 
spinal cord may be recognized adhering to the inner layer of the 
pia mater. This condition is called myelomeningocele. Spinse 
bifidse usually appear in the sacral or lower lumbar region, and are 
probably due to imperfect closure of the vertebral arches. 

HYDROMYELIA AND SYRINGOMYELIA. 

Hydromyelia is a condition in which the central canal of the 
spinal cord is dilated. It frequently occurs in circumscribed 
portions and is apparently without clinical significance. More 
rarely the whole canal has a microscopic lumen throughout its 
entire length, particularly in cases of hydrocephalus, although in 
the majority of cases of this latter disease the spinal cord is not 
involved. A patulous canal can be distinguished from a patho- 
logic cavity by the fact that the cavity is lined by the normal 
cuboidal epithelium of the ependyma. Usually there is a consid- 
erable collection of ependymal cells in the neighborhood of the 
central canal, and this is more apt to be the case if it is dilated or 
otherwise altered than if it is normal. Occasionally the central 
canal is doubled. This rarely happens throughout the whole 
length of the cord, but is more frequently found in a limited 
portion, especially the lumbar region. This doubling is due in 
some instances to the obliteration of the central part of a dilated 
canal with its long axis transversely placed. Sometimes a slit- 
like canal shows a dilatation in only one part. Sometimes the 
lumen of the canal is completely obliterated, leaving nothing but 
a mass of cells in the gray commissure, in the midst of which 
capillaries may be observed. More distinct pathologic changes 
are the diverticula that occasionally spring from the canal. These 
seem to be most frequent in the cervical and dorsal regions. They 
usually extend downward, and are situated posteriorly to the gray 
commissure. It is possible that collections of epithelial cells from 
the ependyma under similar circumstances may form masses in the 
posterior column without distinct cavity-formation, although this 
is doubtful. These changes are particularly significant on account 
of their relation to the disease known as syringomyelia (Fig. 357). 

Syringomyelia. — Pathologically this is essentially a cavity 
in the spinal cord that is not lined throughout with the columnar 
epithelium of the ependyma. This cavity may appear as a wide 



806 



TEXT-BOOK OF PATHOLOGY. 



dilatation or as a narrow slit. It usually occupies the posterior 
part of the cord, is exceedingly asymmetrical, sometimes limited 
entirely to one side, and in these cases is ordinarily found in the 
posterior horn or on its inner side. The cord may be unaltered 
externally. The dura mater is commonly normal. The pia 
and arachnoid are either normal or else thickened slightly, the 
change being not unlike that found in senility or in cases of 
chronic edema of the membranes. The shape of the cord may be 
entirely normal. This, however, is rare. Usually there is some 
asymmetry, and frequently, particularly if the cavity is large, the 
cord upon being removed and laid upon a flat surface seems to 
collapse, giving rise to the so-called ribbon-appearance. Section 
through the cord shows the existence of a larger or smaller cavity 
filled with the products of liquefaction-necrosis, cerebrospinal 
fluid, or else more rarely with blood. Sometimes it appears to 
have been empty, in w r hich case the cord probably was collapsed 




Fig. 357.— Hydromyelia (partly diagrammatic). 



in the spinal canal, and the space thus formed was filled with 
cerebrospinal fluid. The solid portion of the cord is usually some- 
what darker in color, and the distortion of the outline corresponds 
to the extent of the process. The portions of spinal cord not 
involved by the lesion, and below it, commonly show more or less 
descending degeneration. In the portion above the cavity, if it 
does not extend as far as the medulla, some degeneration in the 
posterior columns is often found. In many cases, however, both 
the ascending and descending tracts are intact; at least they appear 
so to the naked eye. Microscopic examination shows that the 
cavity is bounded, as a rule, by a delicate reticulum of neuroglia. 
Sometimes this is lined with what appears to be connective tissue, 
and is supposed to be an inclusion of the pia mater. At other 
times it is lined with ependymal epithelium ; occasionally, as has 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 807 



been previously mentioned, it may contain blood. The tissue in 
the neighborhood is usually hyperplastic neuroglia. The fibers are 
coarse ; the cells are sometimes swollen, sometimes shrunken, and 
show various signs of commencing degeneration. They may be 
numerous or few. The cord in the immediate neighborhood may 
show curiously few changes, the ganglion-cells being perfectly 
normal and the fibers uninjured. If the cavity is extensive and 
the proliferation of the neuroglia considerable, this is not usually 
the case. An entire posterior root may be destroyed, or perhaps 
half or more of the spinal cord, and the nerve-fibers in the neigh- 
boring columns will be extensively degenerated ; in these cases 
secondary degeneration always occurs. Not only the pyramidal 
tracts, but also bundles in the posterior columns degenerate down- 
ward. In a case that I have studied the coma-tract of Schultze 
was beautifully outlined. The nerve-roots are also usually involved, 
and there is descending degeneration along the anterior roots, 
which may be detected also in the nerves. The posterior roots 
may show some degeneration, but this is rare and the cells of the 
spinal ganglia are usually intact. Sometimes there is considerable 
vascular proliferation in these portions of the cords not unlike 
cavernous change. Atypical forms frequently occur. There may 
be extensive gliosis, with small or no cavity-formation ; or the 
cavity may be extensive and the proliferation of the neuroglia 
slight. Occasionally the cavity may communicate with the dilated 
central canal, a condition that has given rise to the supposition 

that it is originally due to some congenital malformation. 
. . . . . 

As syringomyelia is particularly a disease of the central por- 
tion of the spinal cord, the fibers that convey pain and tempera- 
ture-sense are essentially involved, and, as a result, one of the 
characteristic changes is the dissociation of sensation — that is to 
say, persistence of tactile sensation or thermo-anesthesia and anal- 
gesia. In addition, as the cells of the anterior cornua are 
involved, there is degeneration in the muscles that they supply. 

As the great majority of all the cases of syringomyelia are associated 
with hyperplasia of the neurogliar tissue of the spinal cord, it is necessary, 
in order to understand the various theories that have been suggested to 
explain its origin, to briefly consider the more recent investigations in 
regard to this tissue. It is now established that it is ectodermal in ori- 
gin, and due to a proliferation of the ependymal cells lining the central 
canal of the spinal cord and the ventricles of the brain. In the cord these 
cells elongate radially, and the nuclei show active karyokinesis, continuing 
to proliferate until the neuroglia-cells are found in all parts of the spinal 
cord. The cells lining the central canal and, in the human cord, groups of 
cells in its immediate neighborhood, remain cuboidal in shape, and are 
spoken of as ependymal cells. Those cells forming the connective tissue 
of the nervous system are called astrocytes. It was formerly supposed that 
the fibrous portion of the neuroglia was due to the interlacing of the numer- 
ous radiating protoplasmic processes of the latter; although Eanvier and 
Chaslin had both suspected that the fibers were independent of the cells. 



808 



TEXT-BOOK OF PATHOLOGY. 



Since the introduction of the Weigert and the Mallory staining methods, it 
appears certain that, in the human cord at least, the neuroglia-fibers form 
a network independent of the neuroglia-cells. In regard to the origin of 
these cells, it is not certain that they all develop directly from the ependy ma ; 
indeed, it is very likely that the astrocytes may themselves redivide, for 
observations have been made and reported in which their nuclei contained 
karyokinetic figures. Moreover, the repeated proliferation of the neuroglia 
in cases of injury to the central nervous system in situations far removed 
from the primitive ependyma would be an argument in favor of this view. 
Pathologically, various interesting theories have been suggested to account 
for this apparently idiopathic proliferation of the neuroglia. Lenhossek 
believes that besides the fully formed astrocytes other neuroglia-cells remain 
throughout life in a sort of latent condition and represent superfluous ele- 
ments formed during embryonal existence. These, he believes, may, under 
certain circumstances, commence to proliferate and give rise to gliosis. A 
certain amount of neurogliar proliferation appears to be normal in the neigh- 
borhood of the central canal of the human spinal cord, and has already been 
described in the discussion of hydromyelia ; in some cords it may reach 
a very extreme degree, often causing obliteration of the central canal, whose 
place is then taken by an irregular group of cells, in the midst of which 
blood-vessels may be found. Of the various theories that have been sug- 
gested, the most important is that of lymphatic or venous congestion, 
based upon the general dilatation of the perivascular spaces in all instances 
of gliosis. Cases, however, do occur in which this dilatation of the lymph- 
spaces does not exist. A more widely supported theory is that of congenital 
dislocation of some of the ependymal cells of the central canal, either in 
the form of diverticula, or as solid plugs, or as wholly separated cavities. In 
many of the cases of syringomyelia such ependymal cells are found lining 
the abnormal cavity, and in some cases, as has been stated, the syringo- 
myelic cavity communicates with that of the central canal. According to 
this, syringomyelia is only a pronounced modification of hydromyelia. This 
theory is particularly supported by Hoffmann, who draws a distinction in 
the hyperplasia between gliosis and gliomatosis; the former representing 
proliferation of the ependymal cells, and the latter being a neoplastic forma- 
tion, giving rise to elongated tumors with increase in the size of the spinal 
cord. 

Schlesinger also believes that the hyperplasia commences in the epen- 
dymal cells, and that congenital anomalies play a large part in their etiol- 
ogy. Saxer suggests that the neuroglia-cells may have retained some of 
their embryologic properties and be capable of proliferating. Weigert, who 
disbelieves emphatically in the theory of softening of the gliosis, suggests 
that the gliosis, if it exists at all, is possibly secondary. Among the other 
theories are those of softening after traumatism or the result of angioma- 
tous degeneration of the blood-vessels. Gerlach has reported a case in 
which the cavity appeared to be lined with pia mater. It is certain that 
in the great majority of cases there is true proliferation of the neuroglia- 
tissues,the cells being increased in number, and the fibers coarser and forming 
a wide-meshed network around the canal. A true gliomatous formation 
may also occur, and it is not unlikely that syringomyelia is rather a syn- 
drome than a pathologic, or at least an etiologic, entity. 

CIRCULATORY DISTURBANCES. 

Diseases of the walls of the blood-vessels are similar 

to those occurring in the blood-vessels of the other parts of the 
.body. Extensive atheromatous changes are relatively rare. Per- 
haps the most frequent disease is hyaline degeneration. Hyal- 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 809 



ine degeneration is exceedingly common in cases of sclerosis, 
and may occur in early life, even in childhood. It is almost 
invariably present in the cords of persons dying after middle life. 
Round-cell infiltration of the intima (endarteritis) occurs in syph- 
ilis, and also, though less frequently, in tuberculosis. Fibrous 
thickening of the intima and proliferation of the connective tissue 
of the adventitia are common senile changes. 

Attention has been recently directed more particularly to these 
changes on account of the suggestion by Redlich that they are the 
anatomic basis of paralysis agitans. According to him, the 
characteristic changes are endarteritis and periarteritis, with exten- 
sion of the latter process into the surrounding nerve-substance 
and the formation of perivascular insular scleroses. In addition, 
there is often some degeneration in the posterior columns, and 
occasionally in the lateral columns in the cervical and lumbar 
enlargements. The vascular changes, curiously enough, appear 
to be more severe in the posterior horns than in the other parts 
of the cord, and amyloid bodies are nearly always present in these 
regions. However, in examining the cord of a typical case of 
paralysis agitans I failed to find these lesions, while in another 
case, equally characteristic clinically, they were quite pronounced. 
Fiirstner has also reported a case of paralysis agitans without 
spinal lesions. Redlich's views, therefore, are probably incorrect. 

Miliary aneurysms are very infrequent in the spinal cord. 
Aneurysms of the vertebral arteries, however, sometimes involv- 
ing the commencement of the spinal branches, have been reported, 
but are rare. 

Amyloid degeneration is found in cases of general amyloid 
disease. 

Active hyperemia of the spinal cord is rather a clinical 
hypothesis than a pathologic entity. Occasionally, however, the 
gray matter seems to be slightly darker than normal, and there is 
rather free bleeding from the vessels cut transversely. In many 
cases of myelitis the arteries and capillaries may be found dis- 
tended with blood. 

Passive hyperemia is more readily detected in the veins of 
the membranes than in the cord itself. 

Anemia is an important and easily recognized condition. 
Experimentally it has frequently been produced by ligation of the 
abdominal aorta. Cases have occasionally occurred in human 
beings in which, this vessel was occluded by a thrombus, giving 
rise to similar changes. The cord, under these circumstances, 
is somewhat swollen, pale, and soft ; not invariably, however, for 
cases have been reported in which microscopically it was entirely 
normal. The ganglion-cells, particularly those of the anterior 
cornua, are most distinctly affected. They exhibit usually the 
characteristic features of chromolytic degeneration. The proto- 



810 



TEXT-BOOK OF PATHOLOGY. 



plasraic processes become varicose and shortened, and the nucleus 
may be situated at the periphery. Similar changes may occur in 
other portions of the cord, but are exceedingly rare, partly on 
account of the free anastomosis of the blood-vessels, partly be- 
cause if, as sometimes happens, thrombi are formed in the verte- 
bral arteries, death occurs before characteristic changes have had 
time to develop. 

Varicose Veins. — Occasionally a group of vessels in one 
part of the spinal cord will be dilated and varicose, forming a 
sort of plexiform angioma. A condition of this kind has been 
described by Edinger. In this case the vascular plexus had 
evidently developed some time after birth, for there was some 
degeneration of the surrounding nerve-substance, and the patient 
had presented distinct clinical symptoms of pressure in the upper 
part of the cord. Similar angiomatous formations are frequently 
observed in various forms of myelitis and sclerosis. 

Hemorrhages may be of two kinds : punctate and mas- 
sive. 

Punctate hemorrhages are really nothing but pericapillary exu- 
dations of blood-cells, which can readily be distinguished from 
the drops of blood that form at the cross-section of blood-vessels 
by the fact that they cannot be washed off. It is probable that, 
if death does not occur at once, they are in great part absorbed, 
leaving perhaps a minute scar that may be readily overlooked. 
These minute hemorrhages are perhaps more common in the cer- 
vical region than elsewhere. Thev are found in the course of in- 
fectious diseases, particularly those affecting chiefly the nervous 
system, such as tetanus, and especially hydrophobia. Small agonal 
hemorrhages into the substance of the spinal cord, particularly in 
the region of the central canal, are not uncommon. Occasionally 
these may be visible to the naked eye ; they are, of course, to be 
distinguished from ante-mortem changes by the regular form of 
the blood-cells and the absence of blood-pigment. They are only 
important on account of the possibility of their being mistaken 
for pathologic changes. 

Massive hemorrhages may be infiltrating or circumscribed. In 
the former the blood is found between the nerve-fibers and in the 
meshes of the neuroglia. The nerve-substance is usually more or 
less degenerated, and the lesion corresponds anatomically to the 
hemorrhagic infarct. Circumscribed hemorrhages are usually 
small when compared to those in the brain, a circumstance due^ 
of course, to the restricted area in which they can occur. 

The most common cause of this form of hemorrhage is trau- 
matism, and it may sometimes occur as a result of concussion 
without fracture of the spinal column. Hemorrhages may also 
occur in persons with diseased arteries as a result of violent effort 
or emotional disturbance. 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 811 



The clots are usually irregularly oval in outline, and are often 
surrounded by hyperplastic neuroglia, in the midst of which are 
found compound granular cells, and more or less degenerated 
nervous tissue. 

In the later stages the formation of fibrous tissue is apparent ; 
capillaries may also be found bending into the substance of the 
clot, which eventually is absorbed, leaving a scar that nearly 
always contains some pigment surrounded by coarse-meshed 
neuroglia-tissue. Rarely the pigment is absorbed and a cyst re- 
mains. Occasionally the hemorrhagic focus is restricted to the 
gray substance, the blood being found in cylindrical masses. 
This arrangement is due to the fact that in normal circumstances 
the gray matter is softer than the white, and offers less resistance 
to the extravasation of the blood. In this case the infiltrated area 
soon becomes filled with granular cells, the nerve-fibers degener- 
ate, and crystals of hematoidin appear. 

Hematomyelia. — If the central canal is dilated and contains 
blood, the condition is known as hematomyelia. This may occur 
as the result of traumatism or as a result of some vascular de- 
generation. The latter form is occasionally associated with 
syringomyelia, and is found most frequently in the cervical por- 
tion of the cord. If the hemorrhage occurred some time before 
death, the only traces that persist will be discoloration of the 
ependyma, and perhaps the adjacent tissue. Hemorrhage may 
also occur during the death-agony, in which case the central 
canal may either be filled with normal blood-cells, or, if it is 
at all dilated, there will be a thin layer of blood-cells upon the 
surface. The most common situation is at the point where the 
central canal opens into the fourth ventricle. 

INFLAMMATION. 

Myelitis, in the strict sense, is a term signifying an inflam- 
mation of the substance of the spinal cord. According to this 
view, it should be limited exclusively to forms of spinal disease 
secondary to hematogenous infection, extension from the pia, or 
possibly extension from the central canal, although the latter can 
be dismissed as an unknown variety. The name has been used, 
however, to signify any form of softening that may occur, whether 
it be produced by injury or disease of the spinal column, by 
tumors, or by poisons circulating in the blood. It has also been 
applied to secondary changes the result of meningitis and to 
obscure lesions that either commence with a proliferation of the 
neuroglia, or as a primary degeneration or atrophy of the nerve- 
substance and secondary increase in the neuroglia-tissue. 

According to the distribution of the lesions, myelitis is spoken 
of as circumscribed, transverse, or disseminated. Older writers 



812 



TEXT-BOOK OF PATHOLOGY. 



were accustomed to distinguish between those forms which were 
found only in the white matter, those found only in the gray mat- 
ter, and the diffuse forms. The first were known as leukomyeliT 
tis, the second as poliomyelitis, and the third as diffuse myelitis. 
Several varieties may be distinguished by the pathologic character 
of the lesions. 

Hematogenous Purulent Myelitis. — As a rule, the membranes 
of the brain are also infected, and show the characteristic ap- 
pearances of acute leptomeningitis, with subarachnoid accumu- 
lations of pus and injection of the vessels. Cross-section of 
the cord shows here and there small reddish or yellowish 
areas distributed irregularly throughout the cord ; in longi- 
tudinal sections these usually appear as streaks following the 
course of the blood-vessels. The cord often seems to be softer 
and may be darker than normal. The microscopic changes con- 
sist of accumulations of pus in the pia mater and distention of the 
vessels, the presence of a perivascular round-cell infiltration, 
slight degeneration of the nervous tissue in the neighborhood of 
the lesions, and alteration of the neuroglia, which may show some 
looseness of its fibers. Unless the process is advanced, with the 
formation of abscesses of considerable size, or extensive vascular 
change, the true nervous tissue not in the immediate neighbor- 
hood of the foci is but slightly altered. Ordinarily, however, 
alterations may be seen in the ganglion-cells, which consist chiefly 
of irregularity in the arrangement of the chromophilic bodies and 
perhaps somewhat diffuse staining. Should, however, ganglion- 
cells lie in the midst of, or very close to, the purulent focus, they 
show a severer type of degeneration, and often have lost their 
protoplasmic processes. In these cases micro-organisms are not 
infrequently found. In some rare instances the changes in the 
substance may be very pronounced, whilst those in the meninges 
are so slight as entirely to escape macroscopic observation, and to 
be even readily overlooked with the microscope. 

Myelitis secondary to purulent leptomeningitis is not greatly dis- 
similar from this, excepting that there is generally a more marked 
degeneration in the periphery of the cord. The neuroglia-cells 
are increased in this region ; there are often minute hemorrhagic 
foci, and occasionally small peripheral accumulations of pus. 
These lesions have recently been observed, particularly by Coun- 
cilmann, in epidemic cerebrospinal meningitis. 

Transverse myelitis, without local foci, secondary to injury or 
infectious disease — that is, the condition generally denominated 
myelitis — presents three stages, the stage of red softening, of yel- 
low softening, and of gray degeneration. In the first the mem- 
branes of the cord are usually somewhat opaque. The substance 
of the cord itself may be either swollen or shrunken, and is softer 
than normal in consistency. Upon section of the cord the surface 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 813 



is seen to be pink, and there may be minute hemorrhages ; the tis- 
sue swells so that the surface of the cross-section is slightly convex. 
Microscopically the most characteristic feature is the congestion 
of the blood-vessels ; this is more marked in the veins than in the 
arteries. There is usually a considerable amount of perivascular 
cellular exudate, the majority of these cells being polyriuclear leu- 
kocytes. The myelin-sheaths show here and there degeneration ; 
the axis-cylinders are swollen, granular, and somewhat shrunken. 
The neuroglia-cells are sometimes swollen ; sometimes irregular in 
outline and increased in number. The neuroglia-fibers in the 
neighborhood of the vessels form a loose, irregular network. The 
ganglion-cells show pronounced alterations, usually similar to 
those already described as occurring in intoxication, such as 
irregularity in staining, peripheral situation of the nucleus, and 
varicosity or fragmentation of the protoplasmic processes. If the 
process has lasted any considerable time, the most characteristic 
feature of myelitis, namely, the accumulations of granular cells, 
begins to take place. It is not certain what these cells are, but 
in all probability they represent the wandering connective-tissue 
corpuscles that have absorbed the granular fatty detritus of the 
myelin-fibers. Occasionally hyaloid bodies are present, even in 
considerable numbers. These are more irregular in outline than 
those seen in more chronic conditions, and, according to Leyden 
and Goldscheider, are probably due to coagulation of an inflam- 
matory exudate. In the next stage a pressure-anemia begins to 
be apparent. A cross-section through the freshly removed cord 
shows that it is still somewhat swollen ; the color is yellow. The 
distinction between the gray and the white matter is preserved, 
but the gray matter is distinctly shrunken. Microscopically the 
blood-vessels are shrunken ; the perivascular cellular exudate is 
still present, but many of the cells contain fat-droplets. 
Throughout the whole cord are found compound granular cells, 
giving to it a peculiar and characteristic appearance. The nerve- 
fibers are swollen, granular, or shrunken. The myelin-sheaths 
are filled with droplets of fat, or have partially disappeared. 
The neuroglia may be still looser in its texture. The neuroglia- 
cells are more apt to show degenerative changes. In this stage 
the alterations in the ganglion-cells are extreme. They may be 
swollen and irregular; often they form irregular, vacuolar-looking 
masses ; some, however, are shrunken, stain dark, and exhibit no 
trace of a nucleus. Others may perhaps be still recognized by the 
presence of a small vesicle containing the peculiar brownish pigment, 
and finally it is evident that some have wholly disappeared, because 
the number is much less than normal. In the severest grades of this 
condition the substance of the cord has undergone liquefaction and 
is reduced to a puriform mass, which it is impossible to examine, 
excepting upon films. It is then found to contain fat-droplets, 



814 



TEXT-BOOK OF PATHOLOGY. 



granular cells, and detritus. In the stage of gray degeneration 
there is a secondary distention of the blood-vessels, giving it a 
somewhat redder appearance. There is proliferation of the con- 
nective tissue, which has a tendency to retract and cause concavity 
of the surface of the section. The granular cells are found chiefly 
in the neighborhood of the blood-vessels. The neuroglia-tissue is 
looser and appears to inclose numerous vacuoles. The nerve- 
fibers have in large part disappeared, although a few show degen- 
erative changes, and the ganglion-cells are reduced to a few masses 
of pigment or else have disappeared entirely. After the cord has 
been hardened, as also occurs sometimes in various forms of 
sclerosis, cracks may appear in its substance from the retraction 
of the connective tissue. By this time secondary degenerations 
usually begin to appear above and below the lesion, particularly 
in the sections stained by Marchi's method. 

Pressure-myelitis. — The alterations produced in the cord by 
slowly-developing pressure, such as the growth of a tumor in the 
membranes, or gradual bending of the spinal canal, as in Pott's 
disease, produce somewhat characteristic changes. The cord at 
first becomes anemic, due to the mechanical occlusion of blood- 
vessels in the affected segment. As the pressure increases and the 
anemia continues degenerations ensue in the white matter. These 
are accompanied by the appearance of a moderate number of 
granular cells and by slight proliferation of the neuroglia. It 
appears that this degeneration affects first the myelin-sheaths, and 
that the axis-cylinders may maintain their vitality for a consider- 
able length of time ; for regeneration has occurred after the cord 
has been considerably reduced in size by long-continued pressure. 
The gray matter appears to persist for a longer time. This does 
not mean that the ganglion-cells remain absolutely intact, for in 
the early stages of the process they exhibit various degenerative 
changes. As we already know, however, such degenerative 
changes are not necessarily fatal to the vitality of the cell. Later, 
they begin to shrink, usually becoming at first darker, then losing 
their protoplasmic processes, and ultimately undergoing change 
into small irregular vesicles that are frequently pigmented. The 
neuroglia gradually proliferates, and ultimately the cord is con- 
verted into a sclerotic mass at the point of pressure. This mass 
is gray in color, seems dry, and often in the process of hardening 
develops numerous irregular fissures. The central canal is vari- 
ously affected. It may be, at different levels, obliterated, dilated, 
doubled, or even tripled. This appearance of doubling or trip- 
ling, however, is due to the extrusion of diverticula, which pass 
upward or downward more or less parallel to the axis, of the cord. 
The epithelium lining the central canal maintains its vitality to a 
remarkable degree, and, even when all other nervous structures 
have disappeared, stains distinctly and is of normal shape. Fre- 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 815 



quently the endothelium lining the under surface of the pia, or 
the lymph-channels arising from it, proliferate to a remarkable 
degree, and large masses of endothelial cells may be found either 
immediately beneath the pia or more deeply situated in the sub- 
stance of the cord. In some cases this appears to be almost a 
tumor-formation. Secondary degenerations, of course, occur as 
soon as the axis-cylinders begin to swell, and are identical with 
those found in other complete transverse lesions. 

Acute Anterior Poliomyelitis. — In this disease, clinically 
designated infantile palsy, the ganglion-cells of the anterior cornua 
of the spinal cord, their neuraxons passing out through the anterior 
roots, and the muscles over which they have trophic influence, are 
the principal parts involved. The disease is undoubtedly due to 
hematogenous intoxication or infection. It develops after expos- 
ure to cold, subsequent to some other infectious disease, such as 
scarlet fever or measles, and occasionally has appeared as an epi- 
demic. Children are almost exclusively affected, usually about 
the period of the second dentition. The nature of the poison that 
causes it is unknown. 

Microscopically the cord presents no characteristic external 
alterations. If section is made through the diseased portion, it 
can be seen that the tissues of the cord are somewhat redder than 
normal, particularly the anterior cornua of the gray matter, and 
minute hemorrhages may also be observed in this region. The 
tissue is somewhat softer than normal, and the blood-vessels are 
considerably distended. In old cases — that is, those with changes 
consecutive to the cessation of the acute process — the cord may be 
smaller and somewhat denser. Upon section it is readily observed 
that one or both of the anterior cornua are considerably reduced 
in size. The anterior roots from the diseased area may be con- 
siderably shrunken and fibrous. Microscopically, in the early 
stages the most striking appearance is that presented by the blood- 
vessels. These are greatly distended and surrounded by a wall 
of round cells. The vessels in the gray matter of the anterior 
cornua, in the anterior commissure, and in the anterior septum 
appear to be chiefly involved. The posterior half of the cord 
presents few, if any, alterations. The neurogliar tissue seems to 
be somewhat looser, and throughout all the affected tissue there is 
more or less cellular infiltration, the majority of the cells being 
mononuclear. The ganglion-cells are much altered. They 
may be swollen and colorless, the chromatin-granules may be 
arranged in irregular masses, the processes are irregular, the 
nucleus may stain diffusely, and the nucleolus show vacuolar de- 
generation. In the more advanced stages both nucleus and pro- 
toplasmic processes have disappeared, leaving nothing but the 
thickened axis-cylinder springing from the cell. The perivas- 
cular spaces may be somewhat distended, and often contain round 



816 



TEXT-BOOK OF PATHOLOGY. 



cells. Even in cases examined a few days after the onset, it is 
evident that some of the ganglion-cells have degenerated com- 
pletely and have disappeared, as their number is markedly di- 
minished. The fibers of the anterior roots show the ordinary 
forms of degeneration, the presence of globules of fat in the 
sheaths, and swelling or fragmentation of the axis-cylinders. The 
affected muscles very early exhibit fatty degeneration and atrophy 
of the fibers. In cases examined several months after onset 
considerable atrophy has usually taken place in the anterior horns. 
The perivascular round-cell infiltration is still very distinct, and 
usually compound granular cells are found in considerable num- 
bers in the lesions. The ganglion-cells are fewer, and those that 
remain may be either normal or partially degenerated. Many 
fibers have disappeared from the anterior roots, and the trophic 
changes in the muscles are still more pronounced. In those cases 
examined very late — that is, some years after the development of 
the process — the anterior horns appear to be markedly diminished 
in size, although this alteration is exceedingly unequal, often one 
horn being involved whilst the other is perfectly normal or ex- 
hibits only slight alterations. Occasionally the anterior horns 
appear paler, but of almost normal size, apparently the result of 
a colloid degeneration of the neuroglia-tissues. The blood-vessels 
are dilated and their walls thickened, and they may contain some 
cellular infiltration. In those parts where the process is most 
severe all the ganglion-cells have disappeared. In others a few 
may remain, and these are usually normal. The neuroglia has 
undergone hyperplasia, and consists of a coarse meshwork con- 
taining many nuclei. The medullated fibers of the anterior roots 
are partially or completely destroyed. Degeneration of the me- 
dullated fibers of the pyramidal tract may sometimes be traced 
for a few segments above the affected region ; as a rule, it is 
slight, and involves only a few of the fibers. The lesions usually 
attack several segments of the cord, and are most frequent in the 
lumbar region, although any part may be affected, even the cells 
of the medulla. It has been disputed whether the primary 
changes occur in the blood-vessels or in the ganglion-cells, but it 
seems now to be conclusively established that the disease is of 
hematogenous origin. In favor of this view are the pronounced 
vascular changes, and the fact that the ganglion-cells in the neigh- 
borhood of the vessels are usually more degenerated than those 
more remote, and that definite groups of ganglion-cells are not 
affected, but rather those supplied by an individual vascular dis- 
tribution. 

The clinical course of the disease is sufficient evidence of the 
fact that at least some of the cells recover their functions com- 
pletely. After the paralysis has reached its greatest extent, a 
very considerable degree of recovery may ensue, and only certain 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 817 



groups of muscles remain affected. Some of these degenerate and 
contract, giving rise to various deformities in the limbs. 

PRIMARY DEGENERATIONS OF THE CORD. 

Primary degeneration of the spinal cord is characterized by 
the more or less complete destruction of certain systems of fibers, 
affecting their whole length, without solution of continuity in any 
part of their course, or distinct degenerative changes in the gan- 
glion-cells from which they arise. In other words, the distinguish- 
ing characteristic of this condition is the absence of any lesion 
that would serve to explain its occurrence. Certain groups of 
fibers appear to be more frequently affected than others ; these are 
particularly the columns concerned in the conduction of impulses 
from or to the brain. They may be classified as follows : 1. The 
sensory neurons of the cord, which are composed of the unipolar 
cells of the spinal ganglia, and their neuraxons. They pass from 
the posterior roots into the spinal cord, and enter first the column 
of Burdach, subsequently bending into the column of Goll, 
and ending in the nuclei of Goll and Burdach in the medulla. 2. 
The central motor neurons, commencing in the pyramidal layer of 
the motor cortex, passing down through the internal capsule, the 
pyramids, and the pyramidal columns of the cord. 3. The periph- 
eral motor neurons, commencing in the ganglion-cells of the 
anterior cornua, passing out from the anterior groups, and termi- 
nating in the muscles. 

The most important primary degeneration is tabes dor salts, or 
posterior sclerosis; it involves almost exclusively the sensory 
neuron. Involvement of the peripheral motor neuron gives rise 
to the disease known as progressive spinal muscular atrophy ; de- 
generation of both motor neurons, to amyotrophic lateral sclerosis. 

Posterior 5clerosis. 

Degeneration of the posterior columns, when occurring inde- 
pendently of distinct lesions of the posterior roots or section of 
the spinal cord — that is, as a definite form of disease — is known 
as tabes dorsal is, and corresponds clinically to locomotor ataxia. 

There has been considerable discussion of late years as to whether this 
is due to systemic disease attacking primarily certain columns or tracts of 
fibers in the spinal cord, or to a condition secondary to disease of the pos- 
terior roots. The great majority of pathologists have now come to accept 
the latter view, and the evidence in its favor is so strong that it will be here 
adopted. 

Trepinski has recently combated this view, as a result of the comparison 
of the areas of degeneration in certain cases of locomotor ataxia with the 
areas of myelination in the cords of human fetuses. He believes that tabes 
is strictly a systemic disease, and Schaffer partially agrees with him. 
Obersteiner, however, after a careful review of their work, still adheres to 
the theory that the posterior roots are primarily affected. 
52 



818 



TEXT-BOOK OF PATHOLOGY. 



The fibers of the posterior roots appear to originate in the spinal 
ganglia. Upon entering the cord they divide into the ascending and de- 
scending branches, both of which give off collaterals. They may be 
divided into two groups, the lateral and the median bundles, the lateral 
fibers are somewhat finer, and evidently belong embryologically to a dif- 
ferent group, because they acquire their myelin-sheaths later and pass 
directly into the zone of Lissauer, thence into the substantia gelatinosa of 
Rolando, and some of them terminate in arborization about the cells of 
the columns of Clarke. The median bundles, which consist of coarser 
fibers, pass inward, then upward to the inner side of the posterior roots 
then bend in and form the columns of Burdach, and, finally, those from the 
lower regions of the cord enter the columns of Goll and terminate in the 
nucleus and the medulla. Experimental degeneration caused by section of 
the posterior roots in animals, or destruction of the posterior roots as a 
result of pathologic processes in human beings, causes ascending degenera- 
tion of the posterior columns that corresponds very closely in many respects 
to the lesions of tabes dorsalis (Fig. 358). 




Fig. 358.— Sclerosis of the cord ; from a specimen stained by Weigert's method. 

Etiology. — It now seems to be well established that syphilis 
occurs more frequently in the previous history of cases of tabes 
and of general paresis than in the previous history of other forms 
of nervous disease. According to various sets of statistics, it varies 
from 50 per cent, to 90 per cent, in all cases (Erb). Neverthe- 
less, a certain number of cases of tabes occur in persons who give 
no history of syphilis, have never had any symptoms of the dis- 
ease, and present no signs of it at the time of examination. 
Various theories have been suggested to account for the special 
involvement of the posterior columns. Edinger has suggested 
that those portions of the central nervous system that are sub- 
jected to excessive work are more likely than the others to feel 
the action of any toxin that may exist in the body — such, for ex- 
ample, as the toxin of syphilis. Siebert has slightly modified 
this theory, suggesting that at the point where the posterior roots 
enter the spinal cord they are most likely to be subjected to in- 
jurious overgrowth of the neuroglia that may be produced by the 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 819 



presence of toxins, exposure to cold, etc. Hitzig believes that 
toxins may exist in the body for long periods of time, and so 
alter the blood as to cause it to produce in the more susceptible 
portions of the nervous system sclerotic changes. Obersteiner 
has recently suggested that in all probability tabes is due to a 
variety of conditions, although he admits that syphilis is by far 
the most important. As far as we have been able to ascertain, 
only a single case has been recorded in which injury appears to 
have been solely responsible for the development of the disease. 

Pathologic Anatomy. — The macroscopic lesions are as fol- 
lows : The dura shows no changes ; the pia mater in the segment 
between the posterior roots is somewhat thickened and opaque, a 
change which cannot usually be observed in the lateral and anterior 
regions. The posterior roots may be enlarged. In the advanced 
cases, however, they seem to be somewhat thinner and more trans- 
lucent. On section through the cord the gray matter, especially 
that of the septum and anterior horns, appears to be normal. The 
anterior and lateral regions of the white matter are similarly in- 
tact. In the most advanced cases the white matter between the 
posterior roots is darker than normal and seems to be shrunken. 
Its consistency is somewhat softer than that of the normal cord, 
and the fact that it becomes depressed after section shows that 
there is some tendency to retraction. In early cases these changes 
may be slight ; in fact, in cords removed from patients suffering 
from general paresis, in which the earliest stages are usually ob- 
served, there may be no macroscopic changes found. In these 
early stages sections stained by some myelin-method exhibit the 
following changes : In the lumbar region the columns of Goll are 
degenerated, excepting the anterior portion ; usually there is a 
small oval region lying in the middle of the posterior septum ; in 
the dorsal region there are usually two areas of degeneration in 
the column of Burdach ; in the cervical region a portion of GolPs 
column is involved, and there are usually two areas on either side 
in the column of Burdach near the posterior horns. In nearly all 
cases there is usually more or less degeneration of the posterior 
roots. In the more advanced cases the portion of the posterior 
columns immediately behind the posterior commissure contains 
normal fibers, but all the rest of the posterior column and Lis- 
sauer's zone are degenerated. In the cervical portion the degen- 
eration of the column of Goll is most pronounced, and there is 
only a small number of normal fibers anteriorly and on either 
side lying close to the posterior roots. The degeneration extends 
upward through the medulla as far as the nuclei of Goll and Bur- 
dach. It occasionally happens that one portion of the cord seems 
to be more severely affected than the others ; as a general rule, 
this is the lumbar region or the dorsal and lumbar regions, whilst 
the cervical portion shows fewer changes. Occasionally, however, 



820 



TEXT-BOOK OF PATHOLOGY. 



the cervical portion of the cord will be particularly involved and 
the other regions more or less intact. In these cases the columns 
of Goll show only slight degeneration, whilst in the cervical por- 
tion the column of Burdach is markedly degenerated. As the 
fibers turn toward the center, healthy fibers from the posterior 
roots of the cervical segments are usually less involved, so that 
the degenerated area lies near the posterior median septum, in the 
region usually called the middle root-zone. These degenerated 
areas are characterized by destruction of the myelin-sheaths and 
the axis-cylinders, their places being taken by proliferated neu- 
roglia, which is characterized by the appearance of thicker and 
somewhat wavy fibers. In the late stages this hyperplastic neu- 
roglia may undergo considerable contraction (Fig. 359). Pro- 




Fig. 359.— Sclerotic and contracted posterior columns in posterior sclerosis (Karg and 

Schmorl). 

liferation of the neuroglia-cells may be observed in the earlier 
stages, but in the later stages this has largely disappeared. The 
degeneration of the fibers is in all respects similar to that of the 
ordinary secondary degeneration. Accumulation of the peculiar 
amyloid bodies is usually observed. The gray matter of the cord 
is little aifected, the cells in particular rarely showing distinct 
traces of degeneration, although it is not unlikely that more 
careful investigation with the Nissl method will exhibit various 
changes in their finer structure. The fibers that normally pass 
through the gray matter often disappear completely. This is 
true especially of the fine fibers of Lissauer's zone and those 
that form the plexus around the cells of the column of Clarke. 
The reflex collaterals also frequently disappear, and this is sup- 



DISEASES OF THE SPINAL COED AND ITS MEMBRANES. 821 



posed to explain the loss of the reflexes, which is a common 
symptom of the disease. The vessels usually exhibit some thick- 
ening of the adventitia, and occasionally an accumulation of 
granular cells either in the adventitia or beneath the ependyma. 
Hyaline degeneration is found occasionally. The pia mater, cor- 
responding to its macroscopic appearance, shows some thickening 
of the fibers, although it is absent in the earlier cases. 

The most interesting subject connected with this disease is the 
condition of the peripheral nerves, the spinal ganglia, and the 
posterior roots. Degeneration of the peripheral cutaneous nerves 
is frequently observed ; but it is impossible to say, for lack of 
sufficient investigation, whether it occurs in every case. The 
changes consist of thickening of the perineurium and the connec- 
tive-tissue trabecular, more or less degeneration of the myelin- 
sheaths, and occasionally swelling of the axis-cylinders. 

The results of the examination of the spinal ganglia have been 
very contradictory, and some authors find them intact, while 
others describe contraction and irregularity in the outlines of the 
cells. In no case, however, have the changes been sufficiently 
pronounced to account for the extensive degeneration in the poste- 
rior columns. The posterior roots are invariably degenerated. 
Some of the fibers are completely destroyed, others show disap- 
pearance of the myelin-sheaths and alteration of the axis-cylin- 
ders. Nageotte claims to have discovered a round-cell infiltration 
in the membranes surrounding the roots that causes a pressure- 
degeneration. Redlich and Obersteiner believe that the changes 
are most marked after the entrance of the fibers into the cord, and 
explain this by supposing that there has been a slight constriction 
at the point where they pierce the pia mater. In this region 
there is certainly often considerable disappearance of the myelin- 
sheaths, but it cannot be said positively whether the intramedul- 
lary portion of the posterior roots is more degenerated than the 
extramedullary. 

Friedreich's Ataxia. 

Friedreich's ataxia is a disease characterized by inco-ordi na- 
tion of the gait, the first symptoms coming on usually during 
puberty. It belongs to the hereditary type of the disease, occurs 
in successive generations of the same family, and appears to have 
no other causation. The most constant change is hypoplasia 
of the spinal cord. This hypoplasia may be regular, so that the 
whole cord is three-fourths or even less of its normal diameter, 
or it may seem irregular in the latter instance, being, perhaps, 
more pronounced in the cervical and upper dorsal regions. Hypo- 
plasia of the cerebellum is a frequent associated lesion. The two 
conditions are, however, rarely equal, and, according as one or 
the other preponderates, Marie has described spinal and cerebellar 



822 



TEXT-BOOK OF PATHOLOGY. 



forms of hereditary ataxia. The next most common lesion is 
degeneration in the posterior columns. This is particularly 
marked in the column of Goll, but, in severe cases, may also in- 
volve the column of Burdach. No degeneration at all may be 
found ; such a case has been reported by Nonne ; but in these 
instances the larger fibers are usually absent. Degeneration in 
Clarke's columns is not uncommon. The cells exhibit various 
forms of chronic degeneration, and the fibers either disappear 
completely, or at least lose their myelin-sheaths. As a result of 
this latter condition there is also degeneration of the ascending 
cerebellar column. In regard to the degenerative areas found in 
the lateral columns, there is much difference of opinion. The 
majority of authors believe that they represent degeneration of 
the pyramidal columns, although it is certain that none of the 
clinical symptoms associated with this lesion are present. The 
degeneration is usually most pronounced in the lower part of the 
cord, diminishes in intensity upward, and disappears near the nor- 
mal decussation of the pyramidal columns. According to Marie, 
the degenerated areas usually lie to the outer side of the normal 
situation of the pyramidal columns. In all these degenerated 
areas there is considerable proliferation of the neuroglia-tissue, 
the fibers being especially increased, indicating the likelihood that 
the change is secondary. Other secondary changes are the thick- 
ening and partial adhesion of the pia mater, particularly that 
part in contact with the posterior columns of the spinal cord, and 
also the thickening of the walls of the blood-vessels, such as is 
usually found in sclerotic nervous tissue. Degeneration is also 
found in the posterior roots, which are smaller than normal. In 
regard to the condition of the peripheral nerves there is some 
difference of opinion, but it seems certain that, in some cases at 
least, there is a degeneration of the sensory fibers. The disease 
partakes, therefore, of the nature of a combined sclerosis. Some 
authors hold that it is due primarily to a hypoplasia of the third 
primary vesicle and of the neural canal — that is to say, the 
medulla, cerebellum, and cord. The disease, however, appears to 
be slowly progressive, and it is not evident in infancy. This may 
be explained by assuming that the hypoplastic central nervous 
system is sufficient for the needs of the child, and that, as the 
organism develops, it becomes relatively insufficient. This, how- 
ever, would not enable us to understand why such extensive 
secondary degenerations are sometimes present. 



Amyotrophic Lateral Sclerosis. 

Amyotrophic lateral sclerosis is a disease which, theoretically, 
should present the following pathologic changes : Degeneration in 
the pyramidal columns, atrophy of the ganglion-cells of the 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 823 



anterior cornua, degeneration of the nerve-fibers in the anterior 
roots and of the motor fibers in the peripheral nerves, and degen- 
erative atrophy of the muscles. The lesions that are actually 
found, however, are very various. Common to almost all cases is 
the atrophy of the motor cells of the spinal cord and degenera- 
tion of their neuraxons, and the presence of compound granu- 
lar cells, but there is no other sign of inflammatory reaction. The 
degeneration of the ganglion-cells is usually extensive, and the 
muscles exhibit the changes characteristic of progressive spinal 
muscular atrophy — that is, swelling of the fibers, increase of the 
number of the nuclei, indistinctness of the striation, and increase 
in the amount of connective tissue, with, in the later stages, 
extreme atrophy of the fibers. The degree to which the pyram- 
idal columns are affected is not constant; at times the degenera- 
tion is pronounced and extends as far as the internal capsule. 
Indeed, distinct alterations have been reported in the motor cortex 
of the brain— that is to say, degeneration of the ganglion-cells 
and the presence, in more or less considerable number, of com- 
pound granular cells. In other cases the degeneration may cease 
at a lower po'nt, and in at least one case was not found at all. It 
has been supposed that in such cases there is only a slight alter- 
ation in the nutrition of the ganglion-cells, and that the degenera- 
tive changes commence at the peripheral portion of the neuraxon 
and advance cellipetally. The changes found in the pyramidal 
columns are, of course, similar to those occurring in the other 
primary degenerations. 

Combined sclerosis has been described in a great number 
of instances, and a characteristic symptomatology has been ascribed 
to the condition. Usually the parts affected are the posterior 
columns, the columns of Clarke, and, in part, the lateral pyram- 
idal tracts. The lesions do not differ in appearance from those 
of the other forms of primary degeneration. The areas are gray, 
somewhat shrunken, and contain an excess of neuroglia, granular 
cells, and amyloid bodies. The nature of the process is still un- 
decided. The frequency with which a certain definite combination 
occurs has led some neuropathologists to believe that it is a mor- 
bid entity. Others, however, contend that the parts of the cord 
affected are those least able, on account of their poor blood-supply, 
to resist noxious influences, and that, therefore, the disease is only 
the reaction of the weaker parts of the spinal cord to a general 
morbific agent. 

Chronic anterior poliomyelitis, or progressive spinal 
muscular atrophy, is strictly a degeneration of the peripheral 
motor neuron, and often appears to be hereditary in character. 
Otherwise no satisfactory etiology has ever been determined. 
It is characterized by gradual atrophy of the ganglion-cells 
of the anterior cornua and by diminution of the size of the 



824 



TEXT-BOOK OF PATHOLOGY. 



cornua themselves. No lesions that distinctly indicate the 
existence of an inflammatory process are present. The cells 
gradually grow smaller, become pigmented, and may ulti- 
mately disappear. There is degeneration of the fibers in the 
anterior roots and degenerative atrophy of the muscles. The 
clinical course is slowly but irregularly progressive. The con- 
dition in many respects resembles amyotrophic lateral sclerosis, 
and cases have been recorded in which other degenerations were 
found, particularly in Clarke's column and in the posterior col- 
umns. The lesions apparently commence in the cervical region, 
and may later . extend to other parts of the cord, and even to the 
motor nuclei of the medulla. There is a form of chronic polio- 
myelitis in which distinct lesions of the vessels are present, and 
which is apparently only a slow form of the ordinary acute polio- 
myelitis. 

Degenerations in the white matter of the spinal cord 

have been described in various forms of chronic anemia, especially 
pernicious anemia. Two varieties can be distinguished, those in 
which the areas of sclerosis are disseminated irregularly through 
the cord, and those in which the degeneration is systemic in na- 
ture and follows more or less closely the area of distribution of 
the fibers of the posterior root. In the latter case the posterior 
columns are affected most severely, and the lesions are most 
pronounced in the cervical region. Degeneration, however, may 
also be found in the lateral columns, either involving only a 
small patch of fibers, or so extensive as to give rise to the 
appearance of combined sclerosis. The degeneration appears to 
occur primarily in the nerve-fibers, with secondary prolifera- 
tion of the neuroglia. Vascular changes, particularly minute 
hemorrhages and thickening of the vessel-cells, are also found, 
and when present the nerve-fibers in the immediate vicinity of 
the vessels are often degenerated. Lissauer's zone, the posterior 
roots, the spinal ganglia, and the gray matter of the spinal cord 
are rarely involved. These changes are not, however, found in 
all cases of progressive pernicious anemia, a number of cases 
being now on record in which the spinal cord showed no trace 
of degeneration. No satisfactory explanation has hitherto been 
given to account for them. It has been suggested that the anemias 
with spinal lesions belong to a different group, but this is, of 
course, a mere hypothesis. The absence of degeneration in the 
posterior roots seems to exclude a peripheral neuritis, although it 
is possible that in case of slight disease of a spinal ganglia the 
terminations of their nerve-fibers in the medulla would exhibit 
the first trace of degeneration, and this, in fact, corresponds with 
the condition found in some of the cases. 

Similar changes have also been found in other conditions, es- 
pecially the chronic cachexias, such as tuberculosis, diabetes, and 



DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 825 



carcinoma. Tuczek has described changes occurring in the spinal 
cord in ergotism and pellagra. In the former the areas of degen- 
eration were chiefly in the posterior columns, limited, excepting 
in the cervical regions, to Burdach's column, and there were lesions 
in the posterior roots. In the latter disease he found degeneration 
in Goll's column, particularly in Burdach's column, and usually 
in the lateral columns also. There was also partial disappearance 
of the cells of the anterior cornua, and small degenerative foci in 
the anterior columns. Marie believes that these lesions are due 
to degeneration of the endogenous fibers of the spinal cord. 
Changes limited to the posterior column have also been noted after 
diphtheria and leprosy. In old age small, irregular areas of 
degeneration, particularly in the posterior median column, and 
sometimes at the periphery of the spinal cord, may be observed. 

SECONDARY DEGENERATIONS OF THE CORD. 

Secondary degenerations of the spinal cord occur after any 
lesion interrupting the course of one or more of the columns 
of fibers, and also after any disease of the ganglion-cells that 
nourish these fibers. They have been divided into ascending 
and descending, according to the direction in which the de- 
generation proceeds. It will be clear, from the description 
already given of the course of the columns of the cord, that the 
chief variety of descending degeneration will be that of the pyram- 
idal columns. This may occur as a result of injury to the 
motor cortex, or of interruption of the motor fibers in any part 
of their course from the cortex to the conus terminalis. If the 
lesion is unilateral and above the decussation, ordinarily only one 
pyramidal column is distinctly affected — that is to say, the anterior 
pyramidal tract of the same side and the lateral pyramidal tract 
of the opposite side. Careful microscopic investigations, however, 
have shown that certain fibers that do not decussate, pass down 
the spinal cord in the lateral columns. In cases of long-standing 
secondary degeneration of the pyramidal columns a certain amount 
of simple atrophy of the ganglion-cells of the anterior cornua has 
been observed. Descending degeneration has also been observed 
in the posterior columns. In the upper portion of the cord it 
assumes the form of two small areas that project from a point 
slightly posterior to the gray commissure and extend backward 
and outward. This has been called the comma-degeneration of 
Schultze. In the lower part of the cord these descending fibers 
appear to approach the posterior commissure, and form the oval 
field of Flechsig. Descending degeneration for a short distance 
below a total transverse lesion may be found in all the columns. 
Ascending degeneration occurs chiefly in the posterior columns, 
and will be described in connection with tabes dorsalis. In case 



826 



TEXT-BOOK OF PATHOLOGY. 



of isolated injury to one of the posterior roots, there may be 
traced upward a slender band of degeneration that gradually 
approaches the posterior septum. Ascending degeneration also 
occurs in the direct cerebellar tract, and may often be found to be 
associated with disease of the ganglion-cells in Clarke's columns. 
It extends as far as the restiform bodies in the medulla. Ascend- 
ing degeneration also occurs in the anterolateral tract of Gowers. 




Fig. 360.— Sclerosis of the white substance of the cord. 



After total transverse lesion secondary alterations may usually be 
detected in the remote portions of the cord in the course of from 
five to seven days. These alterations consist of a swelling of the 
axis-cylinders and, within a very short time, fatty degeneration 
of the myelin-sheaths. Granular cells appear early in the tissue. 
In the course of a month the degenerative changes are quite pro- 
nounced, and may readily be detected by Weigert's method. The 
myelin-sheaths have disappeared wholly or in part ; the axis- 
cylinders have also vanished, although some varicose fibers may be 
found here and there in the lesion. Compound granular cells 
largely fill the field, but there is also a distinct hyperplasia of the 
neuroglia-tissue, giving the area, microscopically, a somewhat 
grayish appearance. Still later, contraction begins to occur, and 
the appearances seen in the primary degenerations are found. 



DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 827 



TUMORS. 

Glioma. — Of the primary tumors of the spinal cord, the most 
frequent and important is glioma. This is usually infiltrating in 
type and elongated, extending for a distance of several segments 
along the cord, and sometimes involving the nerve-roots, causing 
them to swell and become harder. It may give rise to curious 
distortions in shape, and an apparent hypertrophy ; this latter is 
probably the result of the compression in a longitudinal direction 
of some portion of the cord, so that in a given section more gan- 
glion-cells are found than would normally be present. 

Proliferation of the neurogliar tissue of the cord, causing 
increase in size of the segments affected — often without, however, 
distinctly injuring the normal tissue of the cord — may be pro- 
duced by pressure on the outside or by interference with the 
circulation. It occurs in cases of tumor of the membranes or of 
the spinal column, in disease of the spinal column, and in pachy- 
meningitis. The neuroglia-tissue frequently contains, in addition 
to the increase in the number of fibers, huge multipolar cells that 
have been described in true gliomata by Stroebe. They are best 
shown by Mallory's staining method. 

Sarcoma alone, or containing gliomatous or mucoid tissue, or 
of the type known as angiosarcoma, may also appear. 

Carcinoma and sarcoma may also appear as metastatic 
growths. 

Cysts are exceedingly rare, but both the echinococcus and the 
Cysticercus cellulosse have been reported. 



CHAPTER XIV. 
DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 

THE GANGLIA OF THE CRANIAL AND SPINAL NERVES. 

The ganglia of the cranial nerves may be diseased as a 
result of extension of pathologic processes, usually tuberculosis, 
from the surrounding bony structures. It is probable that they 
are also subject to inflammatory changes. Spiller and Keen have 
reported the results of the examination of a number of Gasserian 
ganglia removed on account of persistent trifacial neuralgia, in 



828 



TEXT-BOOK OF PATHOLOGY. 



which they found degeneration — in some cases total — of the 
my elm-sheaths and the nerve-fibers in the ganglia. In one case 
the degenerated nerve-tissue was replaced by connective tissue, 
giving rise to marked sclerosis. Occasionally the cells in the 
ganglia had undergone atrophy, and in all instances the vessels 
were distinctly sclerotic, the lumen being sometimes completely 
obliterated. The authors believe that these changes are not pri- 
mary, but secondary to lesions in the peripheral sensory nerves. 

The Spinal ganglia may also be diseased. Slight degenera- 
tive changes have been noted in locomotor ataxia and as a result 
of peripheral neuritis. In this case the Avails of the ganglia show 
swelling and granulation of the chromatin-bodies, and are often 
somewhat shrunken. More frequently the ganglia are involved 
as a result of disease of the surrounding bones ; particularly caries 
or sarcoma of the spine may produce pressure, resulting in 
atrophy, or, in the case of the former, areas of tubercular 
softening. The ganglia of the spinal nerves are sometimes found 
diseased in ca^es of herpes zoster, and are supposed to have an 
etiologic relation to that disease. Zinno has reported a case in 
which there appears to have been a chronic swelling of the ganglia, 
some of which were as large as a pigeon's egg, as a result of a 
hyperplasia of the neuroglia and the connective tissue. These 
swollen ganglia pressed upon the cord and produced secondary 
degenerations. Enlarged spinal ganglia have also been observed 
in acromegaly. 

THE NERVES. 
CIRCULATORY DISTURBANCES. 

Hyperemia of the nerve-trunks attends acute inflammations. 
The vessels of the perineurium may be intensely injected. 

Hemorrhages may result from acute congestion or from 
traumatic injuries. They take the form of punctate ecchymoses 
in the perineurium or endoneurium. 

I£dema of the nerve- trunks may occur in the nerves travers- 
ing areas of inflammation. 

ATROPHY AND DEGENERATION. 

Atrophy of the nerves occurs in consequence of pressure 
upon the nerve or as a result of disease (neuritis) of the nerves. 
It may also result from disease of the central nervous system, 
causing disturbance or destruction of the nuclei of origin of the 
peripheral nerves. Occasionally atrophy arises without definite 
cause in old age. The changes in the nerve are similar to those 
following section of the nerve, and are described under the head- 
ing Degeneration. 

Degeneration. — Injury of a nerve in its course produces 



DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 829 



various manifestations in the nerve-fibers corresponding more s>r 
less to the nature of the destructive agencies. It is obvious that, 
if the nerve be divided by a clean incision, the degenerative 
changes below the point of incision will be less extensive than if 
the destructive agent is severe, such as in cauterization, the crush- 
ing of the nerve-trunk with extensive disintegration, or the re- 
moval of a section of some length. Still milder changes, how- 
ever, may be produced by a ligature that is not drawn tightly 
enough to destroy completely all the nerve-fibers. Degenerative 
changes are less pronounced if there is prompt coaptation of the 
injured ends, or if the continuity of the nerve is not entirely 
destroyed. 

If a nerve is examined immediately after injury, there will be 
found only deformity of the nerve-fibers. This consists in 
dislocation of the myelin and perhaps fibrillation of the axis- 
cylinder, so that it seems to be crushed into and diffused through- 
out the white substance of the nerve-fiber. Within a few hours 
the cells in the myelin-sheath begin to exhibit signs of degenera- 
tion, the chromatin swells, stains more feebly, and may undergo 
fragmentation. At the end of eighteen hours the axis-cylinder is 
usually slightly swollen and its outline becomes irregular. These 
changes, however, are by no means uniform throughout the whole 
nerve ; some parts perhaps being almost normal, and others ex- 
tensively degenerated. Wieting states that the cones of Schmidt- 
Lantermann become evident, and are the first indication of nutri- 
tive disturbance. At the end of thirty-six hours the myelin-sub- 
stance has undergone fatty degeneration, with the formation of 
small globules. These changes are found on both sides of the 
lesion ; on the proximal side extending to the first node of Ran- 
vier, and on the peripheral side extending considerably beyond 
this. At first the changes in both fragments are approximately 
equal, but those in the peripheral end rapidly progress, and soon 
dominate the field. The changes in the peripheral fragment, 
however, are more pronounced near the lesion and diminish to- 
ward the periphery. In the central end there are nearly always 
a few fibers that degenerate as far as the spinal cord, but these are 
the exception. 

REGENERATION AFTER INJURY OF A NERVE. 

The first sign of regeneration is proliferation of the cells 
of the sheaths. Their nuclei exhibit karyokinetic figures, and 
there appears to be an increase in their protoplasmic substance. 
At the same time the cells of the connective tissue also under- 
go multiplication and, to a certain extent, act as phagocytes, 
absorbing the fatty detritus. The protoplasm of the cells of 
the sheath gradually elongates and occupies the situation of the 



830 



TEXT-BOOK OF PATHOLOGY. 



my elm-substance and the old axis-cylinder. There appears to be 
some doubt whether these changes are more pronounced in the 
proximal or distal fragments ; at any rate, the protoplasm of 
the cells of the sheaths on both sides of the lesion seem to 
possess phagocytic properties and to absorb some of the fat and 
detritus resulting from the degenerative changes. The proto- 
plasmic mass usually closes the free ends of the nerve-fibers, 
and assumes a somewhat conical form, not unlike a node of 
Ranvier. This mass appears to be continuous with the partially 
degenerated end of the axis-cylinder. Toward the end of the 
first week the elongated protoplasmic masses in the end of the 
nerve-fibers become somewhat differentiated. In the interior 
may be seen a delicate fibrillated structure that appears to be con- 
tinuous with the axis-cylinder of the nerve ; outside of this is a 
delicate grayish membrane, but both of these structures lie within 
the old myelin-sheath, in as far as it is preserved. There is con- 
siderable dispute among pathologists as to whether the central 
fibrillated mass arises from the pre-existing axis-cylinder or from 
the protoplasm of the cells of the sheath. Stroebe maintains 
the former view, and believes that the axis-cylinder, as soon as a 
supporting and directing skeleton has been formed by the proto- 
plasm of the cells, begins to grow, extending toward the lesion, 
outward along the protoplasmic support. It is certain, at any 
rate, that in the course of time the differentiation becomes so dis- 
tinct that it can be seen that the fibrillated central portion is a 
delicate axis-cylinder continuous with the old one, and that the 
gray mass is becoming the myelin-sheath of the fiber. As 
the new nerve-fibers increase in length they gradually pass 
through the injured area and come in contact with the proximal 
area of the peripheral fragment. In this a somewhat similar, but 
certainly less active, process has been taking place — that is to say, 
the cells of the sheath have undergone proliferation and have 
formed protoplasmic masses at the ends of the fiber. Differentia- 
tion in this protoplasmic mass does not, however, appear to occur 
until the new axis-cylinder reaches it. Gradually the nerve 
approximates more and more closely to the normal appearance, 
the axis-cylinder becoming more distinct and the myelin-sheath 
thicker till it can be said to be re-established. In the course 
of the absorption of the fatty and other detritus, cells accu- 
mulate in the connective tissue of the nerve and between the 
fibers that are filled with fat droplets, which are probably ordi- 
nary compound granular cells. It is questionable, however, 
whether they are derived from the endothelium of the lymph- 
spaces or from the leukocytes, or whether they represent the 
excess of the proliferated cells of the sheath. Somewhat later, 
concentric masses may be found that resemble very closely the 
amyloid or hyaloid bodies of the central nervous system. In the 



DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 831 



study of these subjects, as in the study of the details of all the 
finer structures of the nervous system, much depends upon the 
freshness of the tissue, the method of fixation, and the stain em- 
ployed. Stroebe used chiefly anilin-blue, which stains the axis- 
cylinder distinctly. Von Biingner employed saffranin. Neither 
method renders it absolutely certain whether the new axis-cylinder 
is formed by the elongation of the pre-existing axis-cylinder or 
from the protoplasm of the cells of the sheath. It seems, a priori, 
reasonable to conclude that if the axis-cylinder does not directly 
elongate and form the new axis-cylinder, at any rate it exercises 
some peculiar trophic influence upon the protoplasm of the cells 
in immediate contact with it, and is the cause of the peculiar 
differentiation into fibrillar substance. It is certain, moreover, 
that as this fibrillar mass grows downward it passes by the nuclei 
of the cells of the sheath, and does not appear to grow by the 
simple conversion of contiguous protoplasm. On the other hand, 
if the lesion has caused destruction of an extensive portion of the 
nerve, so that the new axis- cylinders do not come in contact with 
the peripheral fragment, they cease to grow, forming first an 
irregular mass of fibers with delicate myelin-sheaths, that are 
soon surrounded and compressed by fibrous connective tissue. 
It therefore seems plausible to believe that certain nutritive ele- 
ments are contained in the peripheral segment, which, if they do 
not form the axis-cylinder directly, are at least absolutely essen- 
tial to its growth and vitality. 

INFLAMMATIONS. 

Neuritis may be either acute or chronic. It has also been 
classified as parenchymatous and interstitial ; the former compris- 
ing the degenerations of the nerve-fibers without involvement of 
the connective tissue, and the latter comprising all those forms 
associated with the characteristic signs of an inflammatory proc- 
ess in the connective tissue of the nerve. 

Acute interstitial inflammation, or neuritis proper, may be caused 
by direct extension from an inflammatory focus in the surrounding 
tissue or by trauma, or as the result of some as yet unknown 
poison, which is generally supposed to be rheumatic in nature. It 
may also occur in the course of acute infectious diseases, or as an 
independent condition, as in beri-beri. The inflammatory changes 
occur in the perineurium and the endoneurium. The nerve is 
swollen, soft, and pinkish in color. Microscopically, both the 
perineurium and the trabecular of connective tissue are increased 
in size, the blood-vessels are distended, and there is extensive 
round-cell infiltration. In the acute forms partially degenerated 
fibers with fatty myelin-sheaths and swollen axis-cylinders are 
found very early. The primary change unquestionably occurs in 



832 TEXT-BOOK OF PATHOLOGY. 

the connective tissue, and the nerve-fibers are involved secondarily, 
the myelin-sheaths being the parts first affected. 

Chronic interstitial neuritis may follow the acute form or com- 
mence as an independent condition. The nerve is harder than 




Fig. 361.— Neuritis : longitudinal section, showing degenerated nerve-fibers (black) ; Azou- 

lay's method; X 300. 

normal, the connective tissue is increased, the walls of the blood- 
vessels are thickened and their lumina may be partially obliterated. 
More or less round-cell infiltration is found in the hyperplastic 




Fig. 362.— Chronic hypertrophic interstitial neuritis (case of Dejerine) ; X 100. 

connective tissue, and the nerve-fibers show extensive degenera- 
tion, many of them having disappeared, and the few that remain 
presenting marked morbid changes. Often there is a distinct pro- 
liferation of the cells in the neurilemma. This form of neuritis 



DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 833 



in particular is associated with muscular degeneration, and appears 
to give rise to the type known as the neural form of progressive 
muscular atrophy. Associated changes are often found in the 
spinal cord, and consist of an ascending degeneration in the pos- 
terior columns and more or less alteration of the ganglion-cells. 
In a variety of this disease, described by Dejerine under the name 
of chrcmie hypertrophic interstitial neuritis, there is an actual over- 
growth of the connective tissue, the nerve-trunks forming huge, 
firm cords, several times the normal thickness, that may readily 
be felt beneath the skin. This disease is apparently due to some 
hereditary influence ; two of the three cases, hitherto reported, 
occurring in the same family. Microscopically, the changes con- 
sist of an enormous proliferation of the connective tissue with 
round-cell infiltration, partly about the sclerotic blood-vessels, 
and pronounced degeneration of the nerve-fibers. The muscles 
undergo degenerative atrophy, and there are secondary degenera- 
tions in the spinal cord. 

Suppurative neuritis is nearly always secondary to suppuration 
in the tissue surrounding the nerve. It is characterized by the 
presence of small foci of pus in the connective tissue and softening 
of the nerve-trunk. The nerve-fibers degenerate very rapidly. 

Parenchymatous neuritis is characterized by a primary degener- 
ation of the nerve-fibers, the alterations in the connective tissue 
being secondary. It is always due to some toxic or infectious 
substance circulating in the fluids of the body. The most common 
causes are lead, arsenic, alcohol, and diphtheria ; but it also occurs 
as a result of other poisons and infectious diseases, and in the 
course of tabes dorsalis. The nerve-trunk becomes slighter, 
firmer, and grayer. Inflammatory changes are slight or absent, 
while the degeneration of the nerve-fibers is pronounced. Changes 
have frequently been found in the cells in the anterior cornua of 
the spinal cord. 

Polyneuritis does not differ from the isolated form, excepting 
that a number of nerve-trunks in various parts of the body, 
usually the limbs, are affected at the same time. It is most fre- 
quently of the parenchymatous type. 

INFECTIOUS DISEASES. 

Tuberculosis of the nerve-trunks is due to direct extension. 
It most commonly affects the roots of the nerves, and occurs in 
the course of tubercular spinal or cerebral pachymeningitis. The 
connective tissue is first affected, and may contain small cheesy 
foci, in which epithelioid and giant-cells are found. The nerve- 
fibers degenerate secondarily. 

Syphilis also occurs, chiefly in the nerve-roots. It causes 
overgrowth of the connective tissue, particularly in the perineu- 

53 



834 



TEXT-BOOK OF PATHOLOGY. 



rium, with pressure upon and degeneration of the nerve-fibers. 
Gummata are sometimes observed upon the cranial nerves. 

I^eprosy is characterized by the presence, in the connective 
tissue of the nerve-fibers, of large epithelioid cells containing 
vacuoles more or less filled with lepra-bacilli. The bacilli cause 
a certain amount of hyperplasia of the connective tissue, which 
presses upon and eventually destroys the nerve-fibers. The dis- 
ease affects the small cutaneous nerves almost exclusively, and 
causes anesthesia and trophic changes in the skin. 

TUMORS. 

Neuroma. — The tumors embraced by this term have been 
sufficiently described under the heading Neuroma, in Part I. 

Sarcoma is a rare tumor of nerve-trunks. It takes its origin 
from the connective tissues of the nerve. 

Muscle-fibers are sometimes found in intramuscular nerve- 
trunks. They usually exhibit proliferation of the nuclei, but the 
striations remain distinct. Their position has been ascribed to 
errors of development, but it is not certain that they are without 
function. 



INDEX. 



Abdominal pregnancy, 670 
Abnormal cell-division, 100 
Abortion, tubal, 669 
Abrin, poisoning by, 28 
Abscess, 111 

actinomycotic, 260 

alveolar, 691 

of brain, 778 

of heart, 379 

of liver, 607 

of prostate, 689 

of spleen, 344 

of thyroid gland, 576 

of tonsil, 495 

of vulva, 677 

peri typhi i tic, 525 

periurethral, 633 

retropharyngeal, 493 

submucous, of intestine, 522 
Absolute immunity, 205 
Accessory suprarenal bodies, 582 
Acervuloma, 156 
Acervulus cerebri, 798 
Acetonuria, 625 

Achromatic substance of nerve-cell, 753 
Acid-intoxication, 35 

cryptogenic, 36 

etiology of, 36 

experimental, 35 

in man, 35 

symptoms of, 36 
Acid-stain, definition, 315 (note) 
Acne, pancreatic, 567 
Acquired immunity, 205 
Acrania, 748 
Acromegaly, 705 

relation of pituitary body to, 797 
Actinomyces streptothrix, 258 
Actinomycosis, 258 

of brain, 791 

of heart, 391 

of intestines, 533 

of lungs, 472 

of mouth, 489 

of muscles, 730 

of pericardium, 396 

of thyroid gland, 579 
Actinomycotic abscesses, 260 
Active hyperemia, 48 

immunity, 205 
Acute yellow atrophy of liver, 544 
Addison's disease, 584 
Adenia, 144 
Adenin, 37 
Adenocarcinoma, 168 

of stomach, 514 



Adenocystoma of ovaries, 658 
Adenoma, 166 
alveolar, 167 
cystic, 169 
destruens, 168 
malignant, of stomach, 514 
of intestines, 533 
of kidney, 609 
congenital, 609 
papuliferous cystic, 610 
of liver, 554 
cystic, 556 
of mammary gland, 698 
of pituitary body, 797 
of suprarenal bodies, 584 
of testicle, 687 
of thyroid gland, 580 
of uterus, 652 

malignant, 652 
of vulva, 678 
racemose, 167 
tubular, 167 
Adenomatous proliferation of glands of 

stomach, 511 
Adenosarcoma, 168 
I of kidney, 609 
! of testicle, 687 
| Adhesions, formation of, 115 
j Aerobic bacteria, 196 
Afanassiew, bacillus of, 273 
Affentuberculose, 348 
Agar-agar, 197 

Age in the etiology of carcinoma, 171 
"Ague-cake," 344 
a-granules, 314 
Air-embolism, 54, 57 
Albuminoid degenerations, 73 
Albuminous infiltration, 66. See Cloudy 

swelling. 
Albuminuria, 626 
Albumose, poisoning by, 30 
Albumoses, formation of, 36 

in blood, effect of, 37 
Albumosuria. 626 

enterogenic, 626 

from extensive burns, 21 

hematogenic, 626 

pyogenic, 627 
Alcohol, poisoning by, 30 
Aleukemic lymphadenoma, 145 
Alexins, 205 

Alimentary glycosuria, 39 
Alkaloids, poisoning by, 30 
Alloxin bases, 37 
Alveolar abscess, 491 
adenoma, 167 

835 



836 



INDEX. 



Alveolar angiosarcoma, 151 

sarcoma, 150 
Ameboid movements of red blood-cor- 
puscles, 318 
Amido bodies in urine, 36 
Amnion, 672 
Amceba cachexica, 288 
coli, 278 

in liver, 506 
urinalis, 279 
Amphistoma bominis, 310 
Ampbitrichous bacteria, 192 
Amyelia, 804 
Amyelinic neuroma, 161 
Amylaceous bodies of prostate, 690 
Amyloid degeneration, 74. See Degener- 
ation. 
of arteries, 398 
of choroid plexus, 790 
of beart, 375 
of intestines, 519 
of kidney, 606 
of liver, 545 

of lymphatic glands, 348 

of muscles, 729 

of pancreas, 564 

of pituitary body, 796 

of spleen, 345 

of submucosa of stomach, 509 
of suprarenal bodies, 583 
of uterus. 649 

formations, local, 75 

material, composition of, 74, 76 
Amyotrophic lateral sclerosis, 822 
Anaerobic bacteria, 196 

cultures, 199 
Anal fissure, 522 
Anastomotic aneurysm, 407 
Anemia, 327 

collateral, 49 

direct, 49 

local, 49 

lymphatic, 144 

of brain, 767 

of heart-muscle, 374 

of kidney, 586 

of liver, 539 

of lungs, 431 

of mucous membrane of mouth, 484 

of muscles, 725 

of pharynx, 492 

of pia, 734 

of spinal cord, 809 

of spleen, 342 

of stomach, 502 

primary, 329 

progressive pernicious, 331 

secondary, 327 

splenic, 329 
Anemias, classification of, 327 
Anemic infarcts, 55 
Anencephaly, 750 
Anesthetic leprosy, 246 
Aneurysm, 404 

associated conditions in other parts 
with, 409 

cirsoid, 407 



Aneurysm, cylindrical, 407 
definition of, 404 
dissecting, 406, 409 
ectatic, 406 
etiology of, 404 
false, 404, 411 
fusiform, 406 
miliary, 406 
of arteries of brain, 765 
of heart, 390 

pathologic anatomy of, 406 
saccular, 407 
spindle-shaped, 406 
spurious, 404, 411 
true, 404 
varicose, 411 
Aneurysma racemosum seu cirsoideum, 
140 

Aneurysmal varix, 411 
Angina, 492 

herpetic, 492 

Ludwig's, 493, 498 
Angiolipoma, 141 

Angioma, 139. See also Hemangioma. 

cavern osum, 140 

of bone, 716 

of liver, 553 

of penis, 681 

of spleen. 347 

telangiectaticum, 139 
Angioneurotic edema, 63 
Angiosarcoma, 146, 151 

alveolar, 151 

myxomatodes, 153 

of dura mater, 733 

plexiform, 151 
Angiosclerosis, 400 
Anguillula intestinalis, 304 

stercoralis, 304 
Anhydremia, 321 
Anilin, poisoning by, 29 
Animal parasites, 277 

in etiology of disease, 32 
Ankylosis of joints. 718 
Ankylostoma duodenale, 303 

duodenalis, 537 
Annectant gyri, abnormalities of, 750 
Annelides, 310 
Anteflexion of uterus, 638 
Anteversion of uterus, 638 
Antbracosis, 86 

of lungs, 455 

of lymphatic glands, 350 
Anthrax, 252 

antitoxin of, 255 

bacillus of, 252 

of intestines, 532 

of muscles, 730 

of stomach, 510 
Antistreptococcic serum, 214 
Antitoxin, 207 

action of, 208 

elimination of, 208 

of anthrax, 255 

of diphtheria, 224 

of leprosy, 249 

of tetanus, 258 



INDEX. 



837 



Antitoxin of yellow fever, 273 

Anuria, 624 

Anus, fistula of, 527 

Aorta, stenosis and atresia of, 351 

Aphthous stomatitis, 485 

Aplasia, definition of, 65 

Apoplexia pulmonum vascularis, 431 

serosa, 769 
Apoplexy, 771 
Appendicitis, 524 

catarrhal, 524 

gangrenous, 524 

interstitial, 524 

necrotic, 524 

pathologic anatomy of, 524 
recurring, 526 
relapsing, 526 
results of, 525 
Aqueduct of Sylvius, 745 
Arachnoid, cerebral, 734 

cholesteatomata of, 741 

edema of, 734 

endothelioma of, 740 

hemorrhages into, 734 

inflammation of, 735 

lipomata of, 741 

syphilis of, 740 

teratomata of, 742 

tumors of, 740 
spinal, 800 

inflammation of, 800 

syphilis of, 801 

tuberculosis of, 801 
Argyria, 86 

Arnold on diapedesis, 51 
Arsenic, poisoning by, 27 
Arseniuretted hydrogen, poisoning by, 

29 

Arterial disorders, effect of, on circula- 
tion, 47 

hemorrhage, 50 

hyperemia, 47 
Arteries, 397 

amyloid degeneration of, 398 

anatomic considerations of, 397 

atrophy of, 397 

calcareous infiltration of, 398 

congenital defects of, 397 

fatty degeneration of, 398 

hyaline degeneration of, 398 

hypertrophy of, 397 

hypoplasia of, 397 

inflammation of, 399 

of brain, atheroma of, 764 
colloid degeneration of, 765 
hyaline degeneration of, 764 
syphilis of, 765 

syphilis of, 404 

tuberculosis of, 404 
Arteriocapillary fibrosis, 400 
Arterioliths, 61 
Arteriosclerosis, 400 

from nephritis, 602 
Arteriosclerotic nephritis, 596 
Arteritis, 399 

acute, 399 

productive, 399 



Arteritis, acute suppurative, 399 
Arthritis, 719 

acute, 719 

chronic, 719 
dry, with ulceration, 720 
purulent, 720 
serous, 720 

deformans, 720 

gonorrheal, 634 

gouty, 722 

neuropathic, 721 

rheumatoid, 720 

senile, 720 
Arthropodia, 311 
Arthrospores, 191 
Ascarides in liver, 557 
Ascaris lutnbricoides, 300, 537 

maratima, 301 

mvstax, 301 
Ascites, 569 

chyliform, 569 

chylous, 569 
Asphyxia, 23 

Aspiration -pneumonia, 447, 450 
Asporogenous races, 192 
Association -fibers of brain, 744 
Astrocytes, 792 

Asymmetric karyokinesis, 100 
Atavism, 18 

Ataxia, Friedreich's, 821 
Atelectasis, 439 

congenital, 439 
Atheroma of arteries of brain, 764 
Atheromatous cyst of testicle, 689 

plate, 401 

ulcer, 401 

Atmospheric pressure, decreased, in eti- 
ology of disease, 22 

increased, in etiology of disease, 22 
Atonic dilatation of stomach, 510 
Atrophic cirrhosis of liver, 548 

sclerosis of brain, 761 
Atrophy, 64 
acute yellow, of liver, 544 
brown, 65 

of heart, 386 
definition of, 64 
etiology of, 65 
muscular, myopathic, 718 

neuropathic, 727 
, progressive, 718 

pseudohypertrophic, 729 

simple, 729 
numerical, 65 
of arteries, 397 
of bone, 710 
of bone-marrow, 358 
of gastric glands, 508 
of heart, 386 
of kidney, 603 
of liver, 541 
of lungs, 435 
of lymphatic glands, 348 
of mammary gland, 686 
of mucosa of intestines, 519 
of muscles, 727 
of nerves, 828 



838 



INDEX. 



Atrophy of pancreas, 563 

of prostate, 690 

of spleen. 345 

of stomach, 508 

of testicle, 681 

of tongue and cheeks, 488 

of uterus, puerperal, 649 
seuile, 649 

pathologic anatomy of, 65 
physiology of, 66 

progressive spinal muscular, 823 

simple, 65 
Atropin, poisoning by, 30 
Auricular septum of heart, defects of, 
362 

Auriculoventricular orifices, stenosis and 

atresia of, 362 
Auto-intoxication, definition of, 19 
Autonomous new-growths, 122 
Avian tuberculosis, 245 

Bacillus, 189, 190 

aerogenes capsulatus, 255 
anthracis, 252 
coli communis, 227 
in kidney, 613 
in urine, 628 
diphtherial, 220 

cultivation of, 225 

distribution of, 222 

pathogenicity of, 221 
icteroides, 272 
influenzae, 263 
lactis aerogenes, 214 
leprae, 245 
mallei, 249 
neapolitanus, 227 
cedematis maligni, 251 
of bubonic plague, 264 
of Ducrey, 271 
of dysentery, 527 
of malignant edema, 251 
of syphilis, 266 
of tetanus, 256 

phlegmones emphysematosa?, 255 
pneumoniae of Friedlander, 219 
proteus in urine, 628 

vulgaris, 274 
pyocyaneus, 214 
pyogenes fcetidus, 214, 227 
smegma-, 243 
tuberculosis, 233 

culture of, 234 

demonstration of, 234 

distribution of, 236 

in urine, 628. 

modes of infection by, 236 
toxic properties of, 244 
typhi abdominalis, 224 
cultivation of, 225 
distribution of, 226 
pathogenicity of, 225 
Bacteria, 188 

artificial cultivation of, 197 
etiology of, 195 
cell-contents of, 190 
cell-membrane of, 192 



Bacteria, chemistry of, 193 
classification of, 190 
conditions of growth of, 196 
definition of, 189 
demonstration of, 193 
diseases due to, 209 

classification of, 31 
embolism by, 54 
entrance of, into the body, 32 
functions and products of, 199 
in etiology of disease, 31 
in urine, 628 
local effects of, 203 
morphology of, 190 
of kidney, 612 

of suppuration, entrance of, into bodv 
109 

in suppurative inflammation, 109 
spores of, 191 
staining of, 193-195 
toxic products of, effects of, 203 
poisoning by, 28 
Bacteriacae, 190 

Bactericidal action of body-fluids, 205 
Bacterioprotein, 109 
Bacterium, 190 

coli commune, 227 

termo in urine, 628 
Bacteriuria, 628 
Balanitis, 679 
Balantidium coli, 280 
Ball thrombi, 59, 365 
Basic stain, definition of, 315 (note) 
Bednar's aphthae, 485 
Beggiatoaceae, 190 
Beri-beri, 277 

Bichlorid of mercury, poisoning by, 25 
Bile, pigmentations derived from, 90 
Biliary cirrhosis of liver, 550 
ducts, 558 

dilatation of, 560 

inflammation of, 558. See Cholan 

gitis. 
stenosis of, 559 
tumors of, 561 
Bilirubin-infarcts in urinary tubules, 91 

in urine, 631 

pigmentation by, 90 
Biliverdin pigmentation, 90 
Bilocular heart, 361 
Biology of bacteria, 195 
Black-tongue. 488 
Bladder, 617 

calculi of, 621 

carcinoma of, 623 

changes of position of, 617 

circulatory disturbances of, 618 

cysts of, 624 

dilatation of, 617 

exstrophy of, 617 

fibro-adenoma of, 623 

fibroma of, 623 

hemorrhages of, 618 

hyperemia of, 618 

inflammation of, 618. See Cystitis. 

malformations of, 617 

myoma of, 623 



INDEX. 



839 



Bladder, myxoma of, 623 

papilloma of, 622 

polypoid growths of, 622 

rupture of, 618 

syphilitic ulcers of, 620 

tuberculosis of, 620 

tumors of, 622 
Blastomycetes as a cause of cancer, 288 
" Bleeders," 52 
Blood, auatomy of, 312 

changes in character of, effects of, on 
circulation, 47 

decrease of quantity of, effect of, on 
circulation, 47 

diseases of, 312 

fixation of, 339 

fixed preparations of, examination of, 
339 

foreign bodies in, 338 

fresh, examination of, 338 

increase of quantity of, effect of, on 

circulation, 47 
in chlorosis, 330 
in leukemia, 335 

in progressive pernicious anemia, 332 
methods of examining, 338 
parasites of, 338 
pathologic changes in, 320 
staining of, 339 
Blood-casts, 600 
Blood-corpuscles, red, 312 

alterations of isotonicity of, 319 

ameboid movements of, 368 

formation of, 317 

nucleated, 318 

pathogenic changes in, 317 

pigmentation of, 319 

shape of, 318 

size of, 317 

vacuolation of, 319 
white, 312. See also Leukocytes. 
Blood-crisis, 319 

Blood-current, alterations in, a cause of 

thrombosis, 57 
Blood-destruction, 98 
Blood-formation, 317 
Blood-plaques, 316 
Blood-plasma, 316 
Blood-poisons, 29 

Blood-pressure, increased, a cause of 
edema, 62 

increase of, hemorrhage from, 52 
Blood-serum as a culture-medium, 197 
Blood-vessels, diseases of, hemorrhage 

from, 52 
Bone, anatomy of, 700 

angioma of, 716 

atrophy of, 710 

carcinoma of, 717 

caries of, 710 

cysts of, 717 

development of, 701 

diseases of, 700 

disorders of, development of, 701 
fibroma of, 716 
giant growth of, 705 
hemorrhage of, 706 



Bone, hyperemia of, 706 

hypertrophy of, 705 

hypoplasia of, 710 

inflammation of, 706 

lepra of, 716 

lipoma of, 716 

myxoma of, 716 

necrosis of, 711 

parasites of, 717 

regeneration of, 703 

sarcoma of, 716 

syphilis of, 715 

thrombosis of, 706 

tuberculosis of 712 

tumors of, 716 
Bone-marrow, 357 

atrophy of, 358 

fatty infiltration of, 357 

hypertrophy of, 358 

inflammation of, 358 

mucoid degeneration of, 357 

pigmentation of, 357 
Bothriocephalus cordatus, 300 

cri status, 300 

latus, 299 

liguloides, 300 
Bouillon as a culture-medium, 197 
Bow-legs, 718 

/3-oxybutyric acid, excessive formation 

of, in body, 36, 41 
Brain, abscess of, 778 

actinomycosis of, 785 

anatomy of, 744 

anemia of, 767 

arteries of, 764. See Arteries of brain. 
carcinoma of, 787 
circulatory disturbances of, 766 
congenital abnormalities of, 748 
degeneration of, after hemorrhage, 772 
development of, 742 
diseases of, 731 
edema of, 768 

local, 769 
embolism of, 773 
examination of, 747 
fibroma of, 787 
glioma of, 785 
gummata of, 784 
hyperemia of, 767 

inflammation of, 775. See also Enceph- 
alitis. 

injury to, 766 

lacerated wounds of, 783 

lymphangioma of, 771 

method of hardening, for examination, 
747 

multiple sclerosis of, 781 

osteoma of, 787 

physiology of, 742, 746 

post-mortem degenerative conditions 

of, 751 
primary vesicles of, 742 
psammoma of, 787 
punctate wounds of, 783 
red softening of, 774 
sarcoma of, 786 
sclerosis of, atrophic, 761 



i 



840 



INDEX. 



Brain, sclerosis of, diffuse, 760 
disseminated, 761 
hypertrophic, 762 
lobar, 781 

syphilis of, 784 

thrombosis of, 773 

total absence of, 750 

tuberculosis of, 784 

tumors of, 785 

white softening of, 774 

yellow softening of, 774 
Brain-sand, 798 
Bread-and-butter pleurisy, 479 
Breast. See Mammary gland. 

male, abnormal development of, 694 
Bright' s disease, acute, 590 
Brornin, poisoning by, 25 
Bronchi, anatomic considerations, 425 

anemia of, 425 

congenital malformations of, 425 

dilatation of, 428 

foreign bodies in, 430 

hemorrhages of, 425 

hyperemia of, 425 

inflammations of. 425 

parasites of, 413 

stenosis and obstruction of, 428 

syphilis of, 429 

tuberculosis of, 429 

tumors of, 429 

ulcers of, 428 
Bronchiectasis, 428 

atelectatic, 440 

cylindrical, 429 

fusiform, 429 

saccular, 429 
Bronchiolitis, 449 

exudativa, 428 
Bronchitis, 425 

acute catarrhal, 426 

capillary, 449 

chronic catarrhal, 426 

fetid, 426 

fibrinous, 427 
Bronchogenic pneumonia, complications 
in, 466 

purulent pneumonia, 456 

tuberculosis of lungs, 459, 460 
Bronchopneumonia, catarrhal, 446 
etiology of, 446 
pathogenesis of, 449 
pathologic physiology of, 447 
pseudolobar form of, 449 
simple, 447 
Bronchorrhea, 426 
Brown atrophy, 65 
of heart, 386 

induration from hyperemia, 49 
Bubo, 351 

syphilitic, 267 
Bubonic plague, 264 
bacillus of, 264 
Bullous emphysema of lungs, 437 
Bursse, inflammation of, 724 
Bursitis, 796 

Cachectic leukocytosis, 325 



Cachexia strumipriva, 580 
Calcareous infiltration of arteries, 398 

of spinal pia, 800 
Calcicosis, 86 
Calcification, 84 

differentiation of, from ossification, 86 

etiology of, 84 

of choroid plexus, 789 

of kidney, 606 

of lymphatic glands, 349 

of mucosa of stomach, 509 

of muscles, 729 

of spleen, 346 

of testicle, 682 

of thrombus, 60 

of veins, 412 

pathologic anatomy of, 84 

physiology of, 85 

seats of, 85 
Calcium salts, poisoning by, 29 
Calculi in bladder, 520 

mulberry, 621 

pancreatic, 567 

phosphatic, 621 

renal, 614 

uric-acid, 621 

urinary, 621 
Calculus in pelvis of kidney, 614 
Callus, 614 

intermediary, 705 

myelogenous, 704 

periosteal, 704 
Calomel, poisoning by, 27 
Canalization of a thrombus, 61 
Cancer, 170. See Carcinoma. % 

cirrhotic, of liver, 554 

colloid, 181 

diffuse hepatic, 554 

endothelial, 157 

of stomach, 511 
Cantharidin, poisoning by, 25 
Capillary bronchitis, 449 

hemorrhage, 50 
Capsule of bacteria, 192 

staining of, 395 
Carbohydrates, disposition of, by the 
body, 39 

value of, in nutrition, 32, 33 
Carbolic acid, poisoning by, 25 
Carbolized thionin, 194 
Carbon-monoxid poisoning, 29 
Carbonates in urine, 631 
Carbonic acid in blood, effect of, 47 
Carbonic-acid gas, poisoning by, 29 
Carcinoma, 170 

animal parasite in, 287 

appearance of, 172 

definition of, 170 

degenerative changes in, 175 

etiology of, 170 

glandular, 179 

medullary, 179 

nature of, 176 

of bladder. 623 

of bone, 717 

of dura mater, 733 

of esophagus, 501 



INDEX. 



841 



Carcinoma of Fallopian tubes, 668 

of intestines, 535 

of kidney, 610 

of larynx, 423 

of liver, 554 

of lungs, 474 

■of lymphatic glands, 357 

of mammary gland, 698 

■of mouth, 490 

•of muscle, 731 

of ovary, 661 

of pancreas, 566 

of penis, 680 

of peritoneum, 574 

of prostate, 693 

of spinal cord, 802 

of spleen, 347 

of stomach, 511 

of suprarenal bodies, 584 

of testicle, 687 

of thyroid gland, 580 

of urethra, 636 

of uterus, 652 

of vagina, 672 

of vulva, 679 

parasites of, 287 

pathologic physiology of, 177 

scirrhous, 179 

seats of, 173 

secondary, 555 

simple, 179 

structure of, 173 

theories as to causes of, 170 

varieties of, 177 
Carcinomatosis, general, 173 
Carcinomatous cylindroma. 182 
Cardioliths, 61 
Caries of bone, 710 

of teeth, 491 
Carnification of lung-tissue, 440 
Caseation, 96 

of testicle, 682 
Casts, blood-, 600 

cellular, 600 

crystalline, 600 

fatty, 601 

granular, 601 

hyaline, 600 

in urine in nephritis. 599 

leukocytic, 600 

waxy, 600 
Catarrh, acute nasal, 418 

mucopurulent, 111 
Catarrhal appendicitis, 524 

bronchopneumonia, 446. See Broncho- 
pneumonia. 

dysentery, 527 

enteritis, 521 

esophagitis, 499 

jaundice, 561 

pharyngitis, 492 

pneumonia, 446 
bacteria of, 219 

stomatitis, 484 

tonsillitis, 494 
Cattle, Texas-fever of, 285 
Caustic ammonia, poisoning by, 25 



Caustic potash, poisoning by, 25 

soda, poisoning by, 25 
Caustics, action of, 25 
Cavernoma, 140 

lymphaticuni, 139 
Cavernous bodies of penis, inflammation 
of, 679 

Cavities, tuberculous, 464 , 
Cecitis, 523 

Cecum, inflammation of, 523 
Cell-contents of bacteria, 190 
Cell-division, abnormal, 100, 117 
Cell-membrane of bacteria, 192 
Cell-multiplication, 117 
Cell-nuclei, degenerations of, 100 
Cells, edema of, 83 

plasma-, 104 
Cellular and attraction theory of inflam- 
mation, 101 

casts, 600 

necrosis, etiology of, 100 
general pathology of, 100 
Central nervous system, injuries of, 783 
Cephalohematoma, 706 

internal, 731 
Cercomonas coli hominis, 279 

intestinalis, 279 
Cerebellum, anatomy of, 745 

hyperplasia of, 750 
Cerebral arteries, 764. See Arteries of 
brain. 

hemispheres, hypoplasia of, 749 
hemorrhage, 769 

degeneration after, 772 
massive, 769 
punctate, 769 
vesicles, primary, 742 
Cerebrospinal fluid, 787 
disease of, 787 
hypersecretion of, 789 
meningitis, epidemic, 737 
Cervix uteri, chronic endometritis of, 
645 

hypertrophy of, 649 

phagedenic ulceration of, 544 

sarcoma of, 652 
Cestodes, 290 
Chalicosis, 455 
Chalmydobacteriacese, 190 
Chancre, 267, 269 

soft, 271 
Chancroid, 271 

of vulva, 678 
Charcot-Neumann crystals of the blood, 
336 

Chauveau's theorv of toxin immunity, 
207 

Cheesy pneumonia, 451 

Chemical conditions, effect of, on growth 

of bacteria, 196 
Chemotaxis, negative, 104 

.positive, 104 
Chilblain, 22 
Chlorin, poisoning by, 25 
Chloroform, poisoning by, 30 
Chloroma, 156, 717 
Chlorosis, 329 



842 



INDEX. 



Cholangitis, 558 

chronic, 559 

results of, 559 

suppurative, 559 
Cholecystitis, 559 
Cholelithiasis, 560 
Cholera, 229, 528 

bacillus of, 229. See Spirillum cholerse 
Asiaticse. 

etiology of, 229 

pathologic physiology of, 231 

spirillum, 229. See Spirillum cholerse 
Asiaticse. 
Cholesteatoma, 187 

of pia and arachnoid, 741 
Cholesterin in fatty degeneration, 73 

in fatty infiltration, 70 

in urine, 631 
Choluria, 625 

Chondrocarcinoma of testicle, 688 
Chondroma, 134 

appearance of, 134 

definition of, 134 

etiology of, 134 

nature of, 136 

of lung, 473 

of mammary gland, 698 
of mouth, 490 
of muscles, 730 
of ovary, 658 
of pleura, 482 
of testicle, 687 
seats of, 135 
structure of, 135 
Chorion, 672 
Choroid plexus, 788 

amyloid degeneration of, 790 
calcification of, 789 
cysts of, 790 
endotheliomata of, 790 
epitheliomata of, 790 
fibroma of, 790 
hemorrhage into, 789 
inflammation of, 789 
pigmentation of, 790 
tuberculosis of, 789 
tumors of, 790 
Chromogenesis, 203 
Chromophilic bodies of nerve-cell, 753 
Chromophoric bacteria, 203 
Chronic inflammation, 111 

relapsing fever, 144 
Chyliform a-cites, 569 
Chylous ascites, 569 

hydropericardium, 392 
Chyluria, 139, 628 
Cicatrices fistuleuse, 466 
Circulation of blood, disturbances of, 45 
Circulatory disturbances, 364 
phenomena, post-mortem, 100 
system, diseases of, 360 
Circumscribed tumors, 125 
Cirrhosis, atrophic, 548 
biliary, 550 
hypertrophic, 549 

Laennec's, 548 
of liver, 547 



Cirrhosis of pancreas, 565 
Cirrhotic cancer of liver, 554 
Cirsoid aneurysm, 407 
Cladothrix, 190 
Clap-threads, 635 
Clau strum, 745 
Cleft palate, 484 
Cloudy swelling, 66 

definition of, 66 

etiology of, 764 

of heart, 374 

of kidney, 604 

of liver, 543 

pathologic anatomy of, 67 

physiology of, 68 
seats of, 68 
Clubbing of finger-ends, 363 
Coagulating ferments, 200 
Coagulation-necrosis, 93 

definition of, 93 

etiology of, 93 

morbid physiology of, 95 

of muscle, 729 

pathologic anatomy of, 94 
Coal-dust pigmentation, 86 
Coal-tar derivatives, poisoning by, 29 
Coccacese, 190 
Coccidium oviforme, 285 

perforans, 286 
Coccus, 189 

Coffee-ground vomit, 503 
Cohnheim's theory as to origin of carci- 
noma, 170 
of tumors, 123 
Cold abscess of joints, 723 
in etiology of disease, 22 
Colitis, 526 

mucous, 526 
Collateral anemia, 49 
hyperemia, 48 
of lungs, 431 
Colloid cancer, 181 
of stomach, 514 
cystomata of ovaries, 658 
degeneration, 81. See Degeneration. 
of arteries of brain, 765 
of pituitary body, 773 
goiter, 577 , 
Colon, inflammation of. 526 
Colpitis, 671 

Combined sclerosis of spinal cord, 798 
Comma-bacillus, 229 
Comminuted fracture, 703 
Commissural fibers of brain, 744 
Compound fracture, 703 

granule-cell, 602 
Concentric hypertrophy of heart, 388 
Concretions beneath prepuce, 681 

in prostate, 690 

in seminal vesicles, 694 

in uriniferous tubules, 607 
Concussion of central nervous system, 783 
Condensing osteitis, 709 
Condyloma acuminatum of penis, 680 

latum, 267, 269 
Congenital cyanosis, 362 

cystic hygroma, 139 



INDEX. 



843 



Congenital rickets, 703 
syphilis, 270 

theory of carcinoma, 170 
Congestion, hypostatic, 46 
Conglutination of blood-plaques, 58 
Connective tissue, fibrous, regeneration 
of, 118 
regeneration of, 119 
Contagious disease, definition of, 31 
Contagium vivum, 31 
Cor bovinum, 388 

villosum, 393 
Cord, spinal. See Spinal cord. 

umbilical. See Umbilical cord. 
Cornutin, 28 

Coronary artery, embolism of, 365 

thrombosis of, 365 
Corpora quadrigemina, 745 
Corpus callosum, congenital absence of, 
749 

fibrosum, 657 

luteum, 657 
Corpuscles of Hassall, 359 
Corrosive chlorid of mercury, poisoning 
by, 27 

poisons, 25 
Coryza, 418 
Cowper's glands, 693 
Cranioschisis, 748 
Craniotabes, 702 
Crenothrix, 190 
Cretinism, 581 
Croton oil, poisoning by, 25 
Croupous enteritis, 522 

laryngitis, 422 

pneumonia, 216, 441. See also Pneu- 
monia. 
Crura cerebri, 745 
Crusta, 745 

Cryptogenic acid-intoxication, 36 
Cryptorchismus, 681 
Crystalline casts, 600 
Cultivation of bacteria, 197 
Culture-media, 197 

inoculation of, 198 
Cultures, anaerobic, 199 
Currant-jelly clots, 364 
Curschmann's spirals, 428 
Cutaneous absorption, pigmentation by, 
88 

Cyanogen-poisoning, 29 
Cyanosis, 48 

congenital, 362 
Cyanotic induration of liver, 539 
of lungs, 433 
of spleen, 342 
Cyclencepbaly, 749 
Cylindrical aneurysm, 407 

bronchiectasis, 429 

cancer of stomach, 514 

epithelioma, 178 
Cylindro-adenoma, 169 
Cylindijoids, 602 
Cylindroma, 152, 169 

carcinomatous, 182 
Cyst-adenoma, 169 

of liver: 556 



I Cysticerci of tape-worm, 291 
racemose, 293 
Cysticercus cellulosae, 557 
j Cystin in urine, 631 
I Cystitis, 618 

mucopurulent, 619 
phlegmonous, 619 
pseudomembranous, 620 
Cysto-adenoma of ovaries, 658 
Cystocele, 642 
vaginal, 670 
Cystoids, 184 

Cystoma of ovary, colloid, 354 
glandular, 658 
myxoid, 658 
papillary, 659 
Cystomata. Same as Epithelial cysts, 184 
Cysts, 183 

classification of, 184 
dermoid, 187 

due to foreign bodies, 184 
epithelial, 184 

of alveolar processes of jaw, 491 

of bladder, 624 

of bone, 717 

of choroid plexus, 790 

of dura, 733 

of Fallopian tube, 668 

of kidnev, 610 

of Kobelt, 662 

of liver, 556 

of lungs, 475 

of mammary gland, 700 

of mouth, 490 

of pancreas, 566 

of parovarium, 661 

of penis, 680 
i of pituitary body, 797 

of prostate, 693 
j of scrotum, 680 

of spinal cord, 827 

of spleen, 347 

of testicle, 688 

of urethra, 686 

of uterus, 655 

of vagina, 672 

of vulva, 679 

proliferation-, 184 

retention-, 184 

softening-, 184 

tubo-ovarian, 668 
Cytorcytes variolar seu vaccinae, 290 

Daughter-stars, 117 
Decidua, 672 

hemorrhage from, 674 
hyperplasia of, 675 
inflammation of, 674 
reflexa, 673 
serotina, 673 
vera, 672 
Defensive proteids, 208 
Degeneration, amyloid, 74 
definition of, 74 
etiology of, 74 
local formations of, 75 
microscopic appearances of, 75 



844 



INDEX. 



Degeneration, amyloid, of arteries, 398 
of heart, 375 
of intestines, 519 
of kidney, 606 
of liver, 545 
of muscles, 729 
of pancreas, 564 
of pituitary body, 796 
of spleen, 345 

of submucosa of stomach, 509 

of suprarenal bodies, 582 

of uterus, 649 

pathologic anatomy of, 74 
physiology of, 76 

reactions for, 75 

seats of, 75 
colloid, 81 

definition of, 81 

etiology of, 81 

of arteries of brain, 765 

of pituitary body, 796 

pathologic anatomy of, 81 
physiology of, 82 
defined, 66 
fatty, 70 

definition of, 70 

etiology of, 71 

microscopic appearances of, 72 

of arteries, 398 

of gastric glands, 508 

of heart, 376 

of kidney, 605 

of liver. 543 

of muscles, 729 

of prostate, 690 

of suprarenal bodies, 582 

of testicle, 682 

of uterus, 649 

of veins, 412 

pathologic anatomy of, 71 
physiology of, 73 

seats of, 73 
hyaline, 76 

definition of, 76 

etiology of, 76 

of arteries, 398 
of brain, 764 

of heart, 375 

of muscles, 729 

pathologic anatomy of, 77 
physiology of, 78 

seats of, 78 
mucoid, 79 

definition of, 79 

etiology of, 79 

microscopic appearances of, 80 

pathologic anatomy of, 79 
physiology of, 80 

seats of, 80 
myxomatous, of mammary gland, 696 

of testicle, 682 
parenchymatous, 66 

of heart, 375 

of kidnev, 604 

of liver, 543 

of muscles, 729 

of pancreas, 564 



Degenerations, 66 

Deglutition-pneumonia, 447 

Dendritic tumors, 125 

Denecke, spirillum tyrogenicum, 232 

Dental osteoma, 138 

Dermatomyositis, 726 

Dermoid cyst, 187 

of choroid, plexus, 790 

of ovary, 660 

of testicle, 689 
Destructive adenoma, 168, 
Determining causes of disease, 19 
Dextrinuria, 625 
Dextrocardia, 361 
S-granules, 315 
Diabete bronze, 42, 88 
Diabetes, 40 
etiology of, 40 

from puncture of medulla, 41 

metabolism in, 41 

pathogenesis of, 40 

pathologic anatomy of, 41 

phosphaticus, 42 
Diacetic acid, excessive formation of, in 

body, 34, 41 
Diaceturia, 625 

Diapedesis of red blood-corpuscles, 51 

in inflammation, 105 
Diaphragmatic hernia, 516 
Diastatic ferments, 200 
Diastematomyelia, 804 
Dichotomy of bacteria, 193 
Diffuse nephritis, 589 
acute, 591 

sclerosis of brain, 760 
Diffusion, escape of fluid by, 61 
Dilatation of bladder, 617 

of Fallopian tubes, 663 

of heart, 387 

of intestines, 515 

of stomach, 509 
atonic, 510 

of ureter, 613 

of uterus, 640 
Diphtheria, 220 

antitoxin of, 223 

bacillus of, 220 

of animals, 222 

of pharynx, 496 

of vulva, 678 

pathologic anatomy of, 222 

physiology of, 223 
toxin of, 223 
Diphtheria-bacilli, non-pathogenic, 221 
Diphtheritic dysentery, 527 
endocarditis, 368 
inflammation, 108 
laryngitis, 422 
membrane, structure of, 108 
rhinitis, 419 
salpingitis, 665 
Diplococcus intracellulars meningitidis 
in leptomeningitis, 735 
pneumoniae, 216 

in diseases other than pneumonia, 
218 

Direct heredity, 18 



INDEX. 



845 



Disease, causes of, 18 
determining, 19 
predisposing, 18 
definition of, 17 
etiology of, 18 
pandemic, 31 
Disorders of nutrition and metabolism, 
32 

Dissecting aneurysm, 406, 409 
Disseminated sclerosis of brain, 761 
Distoma conjunctuni, 310 

crassum, 310 

haematobium, 309 
in kidney, 613 

hepaticuni, 308. 552 

heterophyes, 310 

lanceolatum, 557 

ophthalmobium, 310 

pulmonale, 310 

sinese, 310 
Disturbances of circulation of blood, 45 
Diverticula of intestines, 515 
Diverticulum, Meckel's. 515 
Docbmius duodenalis, 303 
Dracunculus medinensis, 305 
Dropsical infiltration, 83. See Infiltration. 

of liver, 545 
Dropsv from nephritis. 603 

of gall-bladder, 560 ' 

of joints, 719 

of peritoneum, 569 
Dry gangrene, 98 

pericarditis, 392 
Ducrey, bacillus of, 271 
Ductus Botalli. patulous. 362 
Duodenitis, 523 

Duodenum, inflammation of, 523 
Dura mater, 731 

angiosarcoma of. 733 
carcinoma of, 733 
cysts of, 733 
fibroma of, 733 
gliosarcoma of, 733 
hemorrhages of, 731 
hyperemia of, 731 
inflammation of, 731 
spinal, 798 

fatty infiltration of. 798 
fibroma of, 800 
hemorrhage into, 799 
lipoma of, 800 
myxoma of, 800 
sarcoma of, 800 
syphilis of, 799 
tuberculosis of, 799 
tumors of, 799 
syphilis of, 732 
tuberculosis of, 732 
tumors of, 733 
Dust-cells, 453 
Dust-corpuscles, 318 
Dust-embolism, 56 
Dwarf tape-TVorni, 295 
Dysentery, 527 
bacillus of, 627 
catarrhal, 527 
diphtheritic, 527 



Dysentery, gangrenous, 527 

ulcerative, 527 
Dysmenorrhcea membrauacea, 641 
Dyspepsia, 505 

Eccentric hypertrophy of heart, 388 
Ecchondromata, 134 
Eccbondroses, 135 
! Ecchymosis, definition of, 53 
Echinococcus cyst, 297 
of kidney, 613 
of larynx, 424 
of liver, 557 
of peritoneum, 575 
of testicle, 689 
of thyroid gland, 580 
endogenes, 298 
hydatidosus, 298 
multilocularis, 298 
scolicipariens, 297 
Echinorrhyncbus gigas, 307 
Ectatic aneurysm, 406 
Ectogenous teratoma, 186 
Ectoplasm of bacteria, 192 
Edema, angioneurotic, 63 
character of the liquid in, 63 
definition of, 61 
etiology of, 61 
from nephritis, 602 
inflammatory, 63 

malignant, 251. See Malignant edema. 

of brain, 768 
local, 769 

of cells, 83 

of intestines, 520 

of kidney, 587 

of larynx, 420 

of lungs, 433 

of nasal cavities, 418 

of nerves, 828 

of pharynx, 492 

of pia and arachnoid, 734 

pathologic anatomy of, 63 

results of, 64 
Edematous inflammation, 107 

laryngitis, 421 
e-granules, 315 

Ehrlich's classification of leukocytes, 313 
side-chain theory of immunity, 209 
triple stain, 340 

Eimeria hominis, 286 

Electrical currents, effects of, on bacte- 
ria, 196 

influences in etiology of disease, 23 
Elephantiasis congenita mollis, 139 

Graecorum, 245. See leprosy. 

of scrotum, 680 

phlebectatic, 414 

vulvae, 678 
Emboli, 53 

sources and nature of, 53 
Embolism, 53 

air-, 56 

dust-, 56 

fat-, 57 

infective, 56 

of brain, 773 



846 



INDEX. 



Embolism of coronary artery, 365 
of intestines, 520 
of kidney, 588 
of liver, 540 
of lungs, 435 
of muscles, 725 
of spermatic artery, 682 
of spleen, 342 
paradoxic, 54 
results of, 54 
retrograde, 54 
seats of, 54 
Embryonic rests, 123 
Emigration of leukocytes of blood, 50 
Emigration-theory of inflammation, 102 
Emphysema, infectious, 255 
of lungs, 435 
bullous, 437 
interstitial, 435 
senile, 438 
substantial, 436 
vesicular, 436 
vicarious, 436 
Empyema, 479 

of gall-bladder 559 
Emulsifying ferments, 200 
Encephalitis, 775 

acute parenchymatous, 776 
chronic, 781 

primary acute hemorrhagic, 779 
simple acute focal, 776 
suppurative, 778 
Encephalocele, 748 
Encephalomalacia, 773 
End-arteries of Cohnheim, thrombosis 

of, 56 
Endarteritis, 399 

chronica deformans, 400 
obliterans, 403 
of cerebral blood-vessels, 809 
Endemic disease, definition of, 31 
Endocarditis, 366 
acute, 366 

etiology of, 366 
lesions in other organs in, 370 
pathologic anatomy of, 367 
results of, 369 
changes in other organs in, 372 
chronic, 370 
etiology of, 370 
pathologic anatomy of, 370 
diphtheritic, 368 
malignant, 368 
micro-organisms of, 366 
mural, 366 
mycotic, 368 

pathologic physiology of, 372 

septic, 368 

ulcerative, 368 

verrucose, 368 
Endocardium, 360 

diseases of, 366 

inflammation of, 366 
Endogenic neurons, 746 
Endogenous teratoma, 186 
Endometritis, 642 

acute catarrhal, 642 



Endometritis, chronic, 643 
of cervix, 645 

decidualis, 674 

exfoliativa. 641 

glandularis, 643 

interstitialis, 643 
Endoplasm of bacteria, 192 
Endospores, 191 
Endosporium, 191 
Endothelial cancer, 157 
Endothelioma, 157, 416 

of arachnoid and pia, 740 

of choroid plexus, 790 

of lungs, 473 

of pleura, 483 
: Enteritis, 521 

catarrhal, 521 

chronic, 522 

croupous, 522 

etiologv of, 521 

follicular, 521 

pathologic anatomy of, 521 
physiology of, 523 

pseudomembranous, 522 

suppurative, 522 
Enterocystoma, 515 
Enterogenic albumosuria, 626 
Enteroliths, 538 
Enteromycosis, 533 
Enterorrhagia, 53 
| Enzymes, 200 
Eosinophile granules, 314 
Ependymitis, 789 

Epidemic cerebrospinal meningitis, 737 

disease, definition of, 32 
Epididymis, inflammation of, 682 

tuberculosis of, 685 
Epididymitis, 634, 682 

acute, 683 
Epiphysis cerebri, 798 
j Epispadias, 679 
' Epistaxis, 53, 418 
: Epithelial cysts, 184 

perles, 178 
i Epithelioma, 178 

contagiosum, animal parasites in, 289 

cylindrical, 178 

of choroid plexus, 790 

of penis, 680 

of scrotum, 680 

of thymus gland, 359 

squamous, 178 
Epulis, 156, 491 
Equatorial spores, 191 
Ergot, poisoning by, 28 
Erythroblasts, 317 
Erythrocytes, 312 
Erythrocytosis, 324 
Escharotics, action of, 25 
Esophagitis, catarrhal, 499 

phlegmonous, 500 

pseudomembranous, 499 

ulcerative, 500 
Esophagus, anemia of, 499 

carcinoma of, 501 

circulatory disturbances of, 499 

congenital defects of, 499 



INDEX. 



847 



Esophagus, dilatation of, 500 

diverticula of, 500 

inflammation of, 499 

passive congestion of, 499 

perforation and rupture of, 501 

stenosis of, 500 

syphilis of, 501 

thrush of, 501 

tuberculosis of, 501 

tumors of, 501 
Estivo-autumnal fever, parasite of, 283 
Etat crible, 775 

segmentaire, 378 
Ether, poisoning by, 30 
Etiology, definition of, 17 

of disease, 18 
Eustrongylus gigas, 307 
Exfoliative vaginitis, 671 
Exogenic neurons, 746 
Exosporium, 191 
Exostoses, 137, 716 
Experimental acid-intoxication, 35 

glycosuria, 39 
Exposure to general high temperature, 

effects of, 21 
Exstrophy of bladder, 617 
External hernia, 516 
Extra-uterine pregnancy, 668 

Facultative aerobes, 196 

saprophytes and parasites, 196 
Fallopian tubes, 662 

anatomy of, 662 

carcinoma of, 668 

congenital abnormalities of, 662 

cysts of, 668 

dilatation of, 663 

displacement of, 662 

fibromata of, 667 

fibromyomata of, 667 

hematoma of, 663 

hemorrhages of, 663 

hyperemia of, 663 

inflammation of, 664. See Salpingitis. 
lipoma of, 667 

papillomatous elevations of, 667 
sarcoma of, 668 
stenosis of, 663 
syncytioma malignum of, 668 
syphilis of, 667 
tuberculosis of, 666 
tumors of, 667 
False croup, 421 
neuroma, 161 
Fat, in fatty infiltration, staining of, 70 
of body, origin of, 33 
of pancreas, 564 
Fat-crystals in urine, 631 
Fat-embolism, 57 
Fat-necrosis, 97 
Fat-splitting ferments, 200 
Fats, value of, in nutrition, 32, 33 
Fatty acids, origin of, 36 
casts, 601 

contracting kidney, 594 
degeneration, 70. See Degeneration. 
of arteries, 398 



Fatty degeneration of gastric glands, 508 
of heart, 376 
of kidney, 605 
of liver, 543 
of muscle, 729 
of prostate, 690 
of suprarenal bodies, 582 
of testicle, 682 
of uterus, 649 
of veins, 412 
infiltration, 68 
definition of, 68 
etiology of, 68 
of bone-marrow, 357 
of dura mater of cord, 798 
of heart, 375 
of kidney, 606 
of liver, 542 
of mammary gland, 696 
of muscles, 729 
pathologic anatomy of, 69 

physiology of, 70 
seats of, 70 
Febris uudulans, 276 
Femoral hernia, 516 
Fermentation, 200 

thrombosis, 58 
Ferments, coagulating, 200 
diastatic, 200 
effects of, 200 
emulsifying, 200 
fat-splitting, 200 
hydrolytic, 200 
inverting, 200 
oxidizing, 200 
produced by bacteria, 199 
proteolytic, 200 
Fetal membranes, 672 
Fetid bronchitis, 426 
Fetus in fetu, 187 
Fever, blood-changes in, 44 
conservative effects of, 45 
definition of, 43 
effects of, on bacteria, 45 
etiology of, 43 
nature of, 43 

pathologic physiology of, 44 
Fibrin-ferment, poisoning by, 29 
Fibrinous bronchitis, 427 

inflammation, 107 

pericarditis, 392 

pleuritis, 478 

pneumonia, 441 
Fibrinuria, 627 

Fibro-adenoma of bladder, 623 
Fibroblasts, 118 
Fibroid of uterus, 650 
interstitial, 650 
mural, 650 
submucous, 650 
subperitoneal, 650 
phthisis, 465 
polyps of uterus, 650 
Fibroma, 127 

appearance of, 128 
definition of, 127 
etiology of, 127 



848 



INDEX. 



Fibroma, intracanalicular, 129 

rnammse nodulum, 129 

nature of, 130 

of bladder, 623 

of bone, 716 

of brain, 787 

of cboroid plexus, 790 

of dura mater, 733 
of cord, 800 

of Fallopian tubes, 667 

of intestines, 533 

of kidney, 608 

of larynx, 423 

of liver, 553 

of lungs, 473 

of mammary gland, 697 
intracanalicular, 697 

of moutb, 490 

of muscles, 730 

of ovaries, 658 

of penis, 681 

of peritoneum, 574 

of pleura, 482 

of spleen, 347 

of stomach, 510 

of testicle, 687 

of tooth-pulp, 491 

of vagina, 672 

of vulva, 678 

seats of, 128 

structure of, 130 
Fibromyoma of Fallopian tubes, 667 

of vulva, 678 
Fibrosarcoma of ovary, 658 
Fibrosis, general, 114 
Fibrous connective tissue, regeneration 
of, 118 

goiter, 577 

pneumonia, 453 
peribronchial, 455 
perivascular, 455 
pleurogenic, 455 
secondary, 455 
Filaria bronchialis, 307 

conjunctivae, 307 

Demarquayi, 307 

diurna, 307 

hominis oris, 307 

immitis, 307 

in peritoneum, 575 

labialis, 307 

lentis, 307 

loa, 307 

lymphatica, 307 
Magalhsesi, 307 
medinensis, 305 
nocturna, 307 
perstans, 307 
restiformis, 307 
Eomanorum-Orientalis, 307 
sanguinis hominis, 306 
in kidney, 613 
Filariasis, 306 

Filtration, escape of fluid by, 61 
Fissure, anal, 522 
Fistula in ano, 527 
Fixation of blood, 339 



Flagella of bacteria, 192 

staining of, 195 
Fleshy moles, 674 
Fluke-worms, 308 
Foetus in fcetu, 661 
Follicular cysts of ovary, 658 

enteritis, 521 

tonsillitis, 494 

ulcers of intestine, 522 
Food, diminished supply of, 33 

increased supply of, effect of, 33 

necessary constituents of, 32 
Foot-and-mouth disease, 485 
Foreign bodies, changes in tissues around,. 
114 

in blood, 338 
in intestine, 537 
in larynx, 424 
in tissues, 20 
Formative cells, 118 
Fowl-tuberculosis, 245 
Fracture, 703 
comminuted, 703 
compound, 703 
repair of, 703 
Fragilitas ossium, 710 
Friedreich's ataxia, 821 
Frog- face, 751 

Fuchsin bodies of cancer, 288 
Fuchsinophile granules in fatty degen- 
eration, 72 
Fungiform tumors, 125 
Fungoid tumors, 125 
Fungus of testicle, benign, 683 

syphilitic, 687 
Furring of tongue, 485 
Fusiform aneurysm, 406 
bronchiectasis, 429 

Galactocele, 700 
Galactorrhea, 696 
Gall-bladder, 558 

contraction of, 560 

dilatation of, 560 

dropsy of, 560 

empyema of, 559 

inflammation of, 559 

tumors of, 561 
Gall-stones, 560 

Ganglia of cranial nerves, diseases of, 827 
Ganglion, 724 

Ganglionar neuroglioma, 786 
Gangrene, 98 

definition of, 98 

dry, 98 

gaseous, 251 

moist, 98 

of lungs, 458 

of vulva, 678 

primary, 98 

secondary, 98 
Gangrenous appendicitis, 524 

dysentery, 527 

inflammation, 115 

stomatitis, 486 
Gaseous gangrene, 251 
Gastrectasia, 509 



INDEX. 



849 



Gastric glands, atrophy of, 508 
fatty degeneration of, 508 

mucosa, pigmentation of, 508 
Gastritis, acute, 503 

chronic, 503 

hypertrophic, 504 

interstitial, 505 

pathologic anatomy of, 503 
physiology of, 505 

pseudomembranous, 503 

ulcerative, 503 
Gastro-intestinal tract, diseases of, 484 
Gastromalacia, 509 
Gastrophthisis, 505 
Gastroptosis, 509 
Gelatin as a culture-medium, 197 
Gelatinous cancer, 181 
General fibrosis, 114 

pathology, definition of, 17 
Genital pore of tapeworm, 291 
Genu valgum, 718 

varum, 718 
Geographical tongue, 485 
Germinal cells, 743 
■/-granules, 315 
Giant growth of bone, 705 
Giant sarcoma of alveolar process of jaw, 
491 

Giant-cell sarcoma, 154 
Giant-cells of tuberculosis, 239 
Gibraltar fever, 276 
Gin-drinkers' liver, 548 
Glanders, 249 

bacillus of, 249. See Bacillus mallei. 

effect on nasal cavities, 419 

of larynx, 423 

of lungs, 472 

of muscles, 730 

of pharynx, 497 
Glandular carcinoma, 179 

cystomata of ovaries, 658 
Glans penis, inflammation of, 679 
Gleet, 635 
Glioma, 158 

ganglionare, 160 

of eveball, 160 

of hair, 792 

of spinal cord, 827 

of suprarenal bodies, 584 
Gliosarcoma of dura mater, 733 
Gliosis, hypertrophic nodular, 749 
Globular thrombi, 365 
Globulinuria, 626 
Globus pallidus, 745 
Glomerulonephritis, 590 
Glossitis, 484, 487 

hemilateral, 488 

parenchymatous, 487 
Glycemia, 39 

Glycogen, formation of, 39 

staining of, 83 
Glycogenic infiltration, 82. See Infiltra- 
tion. 
of kidney, 606 
Glycosuria, 39, 624 
alimentary, 39 
clinical causes of, 40 



Glycosuria, experimental, 39 
Goiter, 576 

colloid, 577 

definition of, 576 

etiology of, 577 

fibrous, 577 

mechanical effects of, 579 

parenchymatous, 577 

pathologic anatomy of, 577 

secondary changes in, 578 

vascular, 577 
Golgi cells, 746 
Gollasch's mixture, 339 
Gonococcus of Neisser, 215 
Gonorrhea, 632 

bacteriology of, 215 
Gonorrheal arthritis, 634 

tenosynovitis, 634 

urethritis, 635 
Gout, 37 

etiology of, 38 

Kalisch's theory, 37 

pathogenesis of, 38 

pathologic anatomy of, 38 
Gouty arthritis, 722 

nephritis, 596 

tophi, 38, 722 
Gram's method of staining bacteria, 194 
Granular casts, 601 
Granulations, 113 
Granule-cell, compound, 602 
Granules of the leukocytes, 314-316 
Granuloma fungoides, 156 
Grape-sugar in blood and urine, 39 
Graves' disease, 582 
Grawitz, slumbering cells of, 105 
Gray hepatization of lung, 444 
Guanin, 37 
Gummata, 267 

of bones, 715 

of brain, 784 

of lungs, 470 

of lymphatic glands, 355 

structure of, 237 
Gymnobacteria, 192 

Hairy polyp, 420 
Hansen bacillus leprae, 245 
Hard papilloma, 165 
Harelip, 484 

Healing by first intention, 113 

by granulations, 113 

by immediate union, 112 

by second intention, 113 
Heart, 360 

abnormality in position of, 361 
in size of, 361 

abscess of, 379 

actinomycosis of, 391 

amyloid degeneration of, 375 

anatomic considerations of, 360 

aneurysm of, 390 

atrophy of, 386 

bilocular, 361 

cloudy swelling of, 374 

congenital diseases and deformities of, 
360 



54 



850 



INDEX. 



Heart, defective development of, 361 
degenerations of, 374 
development of, 360 
dilatation of, 387 
fatty degeneration of, 376 

infiltration of, 375 
hyaline degeneration of, 375 
hypertrophy of, 387 
hypoplasia of, 385 
inflammation of, 379 
parasites of, 391 

parenchymatous degeneration of, 374 
pathologic physiology of, 362 
segmentation of fibers of, 378 
syphilis of, 391 
thrombi in, 59 

thrombosis of cavities of, 364 
trilocular, 361 
tuberculosis of, 391 
tumors of, 391 
wounds and rupture of, 390 
Heart-diseases, effect of, on circulation, 
46 

Heart-muscle, anemia of, 374 

brown atrophy of, 65 

hemorrhages in, 374 

hyperemia of, 374 
Heat, effect of, on growth of bacteria, 196 

in etiology of disease, 20 

local excess of, effect of, 20 
Heat-dissipation, 43 
Heat-production, 43 
Hemangioma, 139 

appearance and seats of, 140 

definition of, 139 

etiology of, 140 

nature of, 142 

of mouth, 490 

structure of, 140 
Hematemesis, 53 
Hematoblast, 366 
Hematocele, retro-uterine, 642 
Hematochromatosis, 519 

of liver, 542 

of pancreas, 564 
Hematochyluria, 306, 618 
Hematogenic albumosuria, 626 

pneumonia, 441 
purulent, 457 

tuberculosis, 467 
Hematogenous pigmentation, 88, 90 

local, 89 
Hematoidin in urine, 631 

pigmentation by, 88 
Hematoma, definition of, 53 

of Fallopian tube, 663 

of vulva, 677 , 
Hematomyelia, 811 
Hematosalpinx, 666 
Hematozoon malarias, 282 
Hematuria, 627 
Hemicrania, 248 
Hemilateral glossitis, 488 
Hemispheres, cerebral, anatomy of, 744 
Hemocytolysis, 323 
Hemofuscin, pigmentation by, 88 
Hemoglobin in urine, 631 



Hemoglobin-derivatives, pigmentatio 

by, 88 
He.moglobinemia, 323 
Hemoglobinuria, 627 

from extensive burns, 21 

paroxysmal, 627 
Herookonias, 318 
Hemolysis, 98, 323 
Hemopericardium, 392 
Hemophilia, 52 
Hemoptysis, 53 
Hemorrhage, 50 

arterial, 50 

by contre coup, 783 

capillary, 50 

causes of, 52, 374 

cerebral, 769 
massive, 769 
punctate, 769 

classification of. 53 

due to disease of blood-vessels, 52 

from increase of blood-pressure, 52 

neuropathic, 52 

of bladder, 618 

of bone, 706 

of bronchi, 425 

of choroid plexus, 789 

of decidua, 674 

of dura mater, 731 
of cord, 798 

of Fallopian tubes, 663 

of heart-muscle, 374 

of intestines, 520 

of joints, 718 

of kidney, 587 

of larynx, 420 

of lungs, 433 

of mammary gland, 695 

of mouth, 484 

of muscles, 725 

of nerves, 828 

of ovary, 656 

of pancreas, 563 

of pericardium, 392 

of peritoneum, 568 

of pharynx, 492 

of pia, 734 

of pituitary body, 796 
of spinal cord, 810 
of spleen, 342 
of stomach, 502 
of suprarenal bodies, 583 
of uterus, 642 
of vagina, 671 
parenchymatous, 50 
per diabrosin, 52 
per diapedesim, 50 
per rhexin, 50 
results of, 53 
traumatic, 52 
venous, 50 
Hemorrhagic diathesis, 52 
diseases, bacteriology of, 274 
infarcts, 53, 55 
of lungs, 434 
inflammation, 115 
myositis, 725 



INDEX. 



Hemorrhagic pachymeningitis, 731 
pericarditis, 394 
pleuritis, 480 
vaginitis testis, 685 
Hemorrhoids, 520 
Hemosiderin, pigmentation by, 88 
Hemothorax, 476 
Hepatitis, 546 

interstitial, acute, 546 

chronic, 547 
parenchymatous, 546 
Hepatization of lungs, 443 
gray, 444 
red, 443 

Heredity as a factor in etiology of carci- 
noma, 172 

as a predisposing factor in disease, 18 

direct, 18 

immediate, 18 

polymorphous, 38 

remote, 18 

theories of, 19 
Hernia, 516 

diaphragmatic, 516 

direct, 516 

etiology of, 516 

external, 516 

femoral, 516 

indirect, 516 

inguinal, 516 

internal, 516 

irreducible, 517 

pathologic anatomy of, 516 

reducible, 517 

retroperitoneal, 516 

strangulated, 517 
Herpetic angina, 492 

laryngitis, 421 
Heteroplastic osteoma, 138 
Heterotopia of gray matter of spinal 

cord, 804 
Hexathyridium pinguicola, 310 

venarum, 310 
Hippuric acid in urine, 630 
Hirudo ceylonica, 310 

vorax, 311 
Hodgkin's disease, 144, 337 
Horseshoe kidney, 585 
Housemaid's knee, 724 
Hutchinson's teeth, 270, 491 
Hyaline casts, 600 

degeneration, 76. See Degeneration. 
of arteries, 398 
of brain, 764 
of heart, 375 
of lymphatic glands, 349 
of muscles, 729 
of spleen, 346 
Hydatid moles, 676 
Hydatids of Morgagni, 668 
Hydremia, 321 
Hydrocele, 682, 684 

funiculi cystica, 685 
spermatid, 685 

processus vaginalis, 685 

spermatica, 684 
Hydrocephalus, 791 



Hydrofluoric acid, poisoning by, 25 
Hydrogen-sulphid poisoning, 29 
Hydrolytic ferments, 200 
Hydrometra, 640 
Hydromyelia, 805 
Hydronephrosis, 614 
Hydropericardium, 392 

chylous, 391 
Hydrophobia, bacteriology of, 274 
Hydrops articulorum, 720 

ex vacuo, 735 

omenti, 569 
Hydrorrhachus, 804 
Hydrorrhcea gravidarum, 673 
Hydrosalpinx, 666 
Hydrothionuria, 625 
Hydrothorax, 477 
Hygroma, congenital cystic, 139 

durse matris, 732 

of pia, 735 
Hyperchromatosis, 100 
Hyperemia, active, 48 

arterial, 48 

collateral, 48 

local, 48 

neuroparalytic, 48 

neurotic, 48 

of bladder, 618 

of bone, 706 

of brain, 767 

of dura mater, 731 

of Fallopian tubes, 663 

of heart-muscle, 374 

of joints, 718 

of kidnevs, 587 

of liver, 539 

of mammary gland, 694 

of mouth, 484 

of muscles, 725 

of nerves, 828 

of pericardium, 392 

of pia, 734 

and arachnoid of cord, 800 

of pituitary body, 796 

of pleura, 476 

of spinal cord, 809 

of spleen, 342 

of testicle, 682 

of uterus, 641 
passive, 641 

of vagina, 671 

of vulva, 677 
passive, 48 

venous, 48 
Hyperglycemia, 39 
Hyperinosis, 320 
Hyperplasia, 121 

of decidual, 675 

of mucous membrane of uterus, 649 

of spleen, 345 
Hyperplastic perihepatitis, 573 
Hyperthyroidism, 582 
Hypertonicity of the blood-serum, 320 
Hypertrophic cirrhosis of liver, 549 

enlargement, 121 

gastritis, 504 

nodular gliosis, 749 



852 



INDEX. 



Hypertrophic sclerosis of brain, 762 
Hypertrophy, 120 

definition of, 120 

etiology of, 120 

numerical, 121 

of arteries, 397 

of bone, 705 

of bone-marrow, 358 

of cervix uteri, 649 

of heart, 387 

with dilatation, 388 

of kidney, 604 

of liver, 551 

of lungs, 435 

of lymphatic glands, 348 

of mammary gland, 696 

of muscles, 724 

of pituitary body, 795 

of prostate, 690 

of testicle, 682 

of uterus, 649 

pathologic anatomy of, 121 
physiology of, 121 

simple, 121 

true, 121 
Hypinosis, 320 
Hypochromatosis, 100 
Hypoleukocytosis, 326 
Hypophysis cerebri, 794. See also Pitui- 
tary body. 
Hypoplasia, definition of, 64 

of arteries, 397 

of bone, 710 

of cerebellum, 750 

of cerebral hemispheres, 749 

of heart, 361, 385 
Hypospadias, 679 
Hypostatic congestion, 46 
of lungs, 432 

pneumonia, 447, 450 
Hypoxanthin, 37 

Icterus, 561. See Jaundice. 

seu febris amantium, 330 
Ileitis, 523 

Ileum, inflammation of, 523 
Ileus, 517 

Immediate heredity, 18 
Immunity, 204 

absolute, 205 

acquired, 205 

active, 205 

Ehrlich's side-chain theory of, 209 

mechanism of, 205 

natural, 205 

passive, 205 

relative, 205 

toxin-, 207 

varieties of, 204 
Inanition, 33 
Indicanuria, 625 
Indigestion, 505 
Indigo in urine, 631 
Indirect cell-division, 117 
Indolent ulcer, 111 
Infarction, 56, 702 
Infarcts, anemic, 56 



Infarcts, formation of, 56 

hemorrhagic, 56 

placental, 674 

pulmonary, 57 

subsequent changes in, 56 

white, 56 
Infection, 203 

Infectious disease, definition of, 31 

embolism, 56 

emphysema, 255 
bacillus of, 255 

leukocytosis, 324 
Infiltrating tumors, 125 
Infiltration, albuminous, 66 

calcareous, of arteries, 398 

defined, 66 

dropsical, 83 

fatty, 68. See Fatty infiltration. 
glycogenic, 82 

definition of, 82 

etiology of, 82 

of kidney, 606 

pathologic anatomy of, 82 
physiology of, 83 
inflammatory, 104 
lymphoid, 144 

medullary, of lymphoid structures of 

intestine, 529 
uratic, 86 
Inflammation, 101 
as a cause of necrosis, 93 
catarrhal, 111 

changes in the blood-vessels in, 103 
chemotactic action in, 104 
chronic, 111 
definition of, 101 

degenerative changes in tissues in, 105 

diphtheritic, 108 

edematous, 107 

etiology of, 107 

exudation in, 103 

fibrinous, 107 

gangrenous, 115 

hemorrhagic, 115 

historical views of, 101 

interstitial, 112 

necrotic, 115 

of appendix vermiformis, 524. See 

Appendicitis. 
of arachnoid, 735 

spinal, 800 
of arteries, 399 

of biliary ducts, 564. See Cholangitis. 

of bladder, 618. See Cystitis. 

of bone, 706 

of bone-marrow, 358 

of brain, 775. See also Encephalitis. 

of bronchi, 425 

of bursse, 724 

of cavernous bodies of penis, 679 

of cecum, 523 

of colon, 526 

of decidua, 674 

of duodenum, 523 

of dura mater, 731 

of epididymis, 682 

of Fallopian tubes, 664. See Salpingitis. 



INDEX. 



853 



Inflammation of gall-bladder, 559 
of ileum, 523 
of intestines, 521 
of joints, 719. See Arthritis. 
of kidney, 588. See Nephritis. 
of larynx, 421 
of liver, 546. See Hepatitis. 
of lungs, 441 
of lymphatic glands, 350 
of lymphatic vessels, 415 
of mammary gland, 695 
of mouth, 484 

of muscles, 725. See Myositis. 

of nasal cavities, 418 

of nerves, 831. See Neuritis. 

of ovaries, 657 

of pancreas, 565 

of pelvis of kidney, 614 

of pericardium, 392 

of peritoneum, 570. See Peritonitis. 

of pharynx, 492 

of pia, 735 

of cord, 800 
of pituitary body, 796 
of placenta, 674 
of pleura, 477 
of prostate gland, 689 
of pulp of teeth, 491 
of rectum, 526 
of salivary glands, 498 
of seminal vesicles, 693 
of spinal cord, 811. See Myelitis and 

Poliomyelitis. 
of spleen, 343 
of suprarenal bodies, 584 
of tendon-sheaths, 724 
of testicle, 682. See Orchitis. 
of thoracic duct, 417 
of thymus gland, 359 
of thyroid gland, 576 
of trachea, 424 
of ureter, 615 
of urethra, 632 
of uterus, 642 

of vagina, 671. See Vaginitis. 

of vas deferens, 685 

of veins, 412 

of vulva, 677 

parenchymatous, 112 

phenomena in, 102 

productive, 111 

proliferative changes in, 105 

resolution after, 115 

round-cell, 104 

serous, 107 

special forms of, 107 

suppurative, 109 

theories of, 101 

types of, 108 
Inflammatory edema, 63 

infiltration, 104 

leukocytosis, 324 

osteoporosis, 709 
Influenza, 263 

bacillus of, 263 
Infusoria, 277 
Inguinal hernia, 516 



Inhibitory action of body-fluids, 205 
Inoculation of culture-media, 198 
Insects, venom of, poisonous effects of, 28 
Insufficiency of heart-valves, 371 
Intermediary callus, 705 
Internal hernia, 516 
Interstitial appendicitis, 524 

emphysema of lungs, 435 

gastritis, 505 

hepatitis, acute, 546 
chronic, 547 

inflammation, 112 

nephritis, 589 
acute, 591 
chronic, 595 

neuritis, acute, 831 
chronic, 832 
hypertrophic, 833 

pregnancy, 668 

uterine fibroids, 650 
Intestinal obstruction, 517 
Intestines, 514 

abnormalities of, 514 

absence of parts of, 514 

actinomycosis of, 533 

active hyperemia of, 520 

adenoma of, 533 

amyloid degeneration of, 519 

anthrax of, 532 

atrophy of mucosa of, 519 

carcinoma of, 535 

circulatory disturbances of, 520 

congenital abnormalities of position of, 
515 

enlargement of, 515 
dilatation of, 515 
distortion of, 514 
diverticula of, 515 
edema of, 520 
embolism of, 520 
fibroma of, 533 
follicular ulcers of, 522 
foreign bodies in, 537 
hemorrhage of, 520 
infectious diseases of, 527 
inflammatory papilloma of, 533 
internal strangulation of, 517 
invagination of, 518 
lipoma of, 533 
myoma of, 535 
myxoma of, 533 
narrowing of, 514, 515 
obstruction of, 517 
parasites of, 536 
passive hyperemia of, 520 
peptic ulcer of, 522 
pigmentation of, 519 
rupture of, 537 
sarcoma of, 533 
stenosis of, 515 
submucous abscess, 522 
syphilis of, 532 
thrombosis of, 520 
tuberculosis of, 531 
tumors of, 533 
ulceration of, 522 
Intoxication, 203 



854 



INDEX. 



Intoxication as a cause of necrosis, 92 
Intracanalicular fibroma, 129 
of mammary gland, 697 
Intussusception, 518 
Invagination of intestine, 518 
Invasion diseases, definition of, 32 
Inversion of uterus, 640 
Inverting ferments, 200 
Involution-forms of bacteria, 192 
Iron-particles, pigmentation by, 86 
Irreducible bernia, 517 
Irregular pneumonias, 219 
Ischemia, 49 

Isotonicity of red blood-corpuscle, altera- 
tions of, 319 

Jaundice, 561 

catarrhal, 561 

etiology of, 561 

pathologic anatomy of, 562 
Joints, ankylosis of, 718 

cold abscess of, 723 

diseases of, 718 

distortion of, 718 

dropsy of, 719 

hemorrhage into, 718 

hyperemia of, 718 

inflammation of, 719. See Arthritis. 
luxation of, 718 
syphilis of, 723 
tuberculosis of, 722 
tumors of, 724 

Karyokinesis, 117 

abnormal, 100 

asymmetric, 100 

multipolar, 100 
Karyokinetic figures in erythroblasts, 
319 

Karyomitosis, 117 
Karyorrhexis, 100 
Keloids, 127 
Kidney, 585 

adenoma of, 609 
congenital, 609 
papuliferous cystic, 610 

amyloid degeneration of, 606 

anemia of, 586 

atrophy of, 603 

bacteria in, 612 

calcification of, 606 

carcinoma of, 610 

circulatory disturbances of, 586 

cloudy swelling of, 604 

congenital anomalies of, 585 

cyanotic induration of, 587 

cysts of, 610 

degenerations of, 604 

echinococcus-cyst of, 613 

edema of, 587 

embolism in, 588 

fatty contracting, 594 
degeneration of, 605 
infiltration of, 606 

fibromata of, 608 

glycogenic infiltration of, 606 

hemorrhages in, 587 



Kidney, horseshoe-, 585 
hyperemia of, 587 
hypertrophy of, 604 
inflammation of, 588. See Nephritis. 
large white, 593 
leiomyoma of, 608 
lipomata of, 608 

lymphomatous infiltration of, 610 
malpositions of, 586 
parasites of, 612 

parenchymatous degeneration of, 604 

pelvis of. See Pelvis of kidney. 

red granular, 596 

rhabdomyosarcoma of, 609 

sarcoma of, 609 

syphilis of, 608 

thrombosis in, 508 

tuberculosis of, 608 

tumors of, 608 
Klebs-Loffier bacillus, 220 
Knock -knee, 718 
Kobelt, cysts of, 662 
Koch's laws for etiologic importance of 
bacteria, 31 

stain for tubercle-bacillus, 235 

tuberculin, 244 

Lactic acid, excessive formation of, in 

body, 36 
Lactosuria, 625 
Lacunar tonsillitis, 494 
Laennec's cirrhosis of liver, 548 
Langhan's cells, 183 
Large white kidney, 593 
Laryngitis, acute catarrhal, 421 

chronic catarrhal, 421 

croupous, 422 

diphtheritic, 422 

edematous, 421 

herpetic, 421 
Larynx, anatomic considerations of, 420 

anemia of, 420 

carcinoma of, 418 

congenital abnormalities of, 420 

echinococcus cysts of, 424 

edema of, 420 

fibroma of, 423 

foreign bodies in, 424 

glanders of, 423 

hemorrhages in, 420 

hyperemia of, 420 

inflammation of, 421 

lepra of, 423 

lupus of, 422 

mucous polyps of, 423 

papilloma of, 423 

parasites of, 424 

syphilis of, 422 

tuberculosis of. 422 

tumors of, 423 
Latent tuberculosis, 243 
Lateral thrombus, 59 

ventricles of brain, 744 
Laveran's malarial parasite, 283 
Lead, poisoning by, 27 
Lecithin in fatty degeneration, 73 

in fatty infiltration, 70 



INDEX. 



855 



Leiomyoma, 161 

of kidney, 608 

of uterus, 650 
Leontiasis leprosa, 247 

ossium, 709 
Lepra, 245. See also Leprosy. 

affections of nasal cavities in, 419 

gangrsenosa, 248 

mutilans, 248 

of bone, 716 

of larynx, 423 

of pharynx, 497 

of testicle, 687 
Lepra-cell, 248 
Leproma, 248 

Leprosy, 245. See also Lepra. 

anesthetic, 246 

antitoxin of, 249 

bacillus of, 245 

etiology of, 245 

of liver, 553 

of nerves, 834 

pathologic anatomy of, 246 
physiology of, 249 

structure of lesions of, 248 

tubercular, 246 
Leptomeningitis, 735 

spinal, 800 
Leptothrix buccalis, 265 
Leucin in urine, 36, 631 
Leukemia, 333 

acute, 337 

blood in, 335 

lienomedullary, 336 

lymphatic, 336 

pathologic physiology of, 337 
Leukemic lymphadenoma, 145 
Leukocytes, 312 

chemical composition of, 316 

emigration of, in inflammation, 103 

large mononuclear, 313 

number of, 316 

origin of, 317 

pathologic changes in, 319 
polynuclear, 314 

proportion of different forms of, 316 

small mononuclear, 313 

transitional, 313 

various forms of, 313 
Leukocytic casts, 600 
Leukocytosis, 324 

cachectic, 325 

infectious, 324 

inflammatory, 324 

medicinal, 325 
Leukolysis, 326 
Leukonuclein, 316 
Leukopenia, 326 
Leukoplakia, 485 
Ley den ia gemmipara, 575 
Lienomedullary leukemia, 336 
Light, effect of, on growth of bacteria, 
196 

Lipaciduria. 625 
Lipemia, 322 
Lipoma, 132 
appearance of, 132 



Lipoma, etiology of, 132 

nature of, 133 

of bone, 716 

of choroid plexus, 790 

of dura mater of cord, 800 

of Fallopian tubes, 667 

of intestines, 533 

of kidney, 608 

of liver, 553 

of lungs, 473 

of mammary gland, 697 

of mouth, 490 

of muscles, 730 

of penis, 681 

of peritoneum, 574 

of pia and arachnoid, 741 

of pleura, 482 

of stomach, 510 

of vulva, 577 

seats of, 133 

structure of, 133 
Lipomatosis, 132 

of mammary gland, 696 
Lipuria, 628 

Liquefaction-necrosis, 95 

definition of, 95 

pathologic anatomy of, 96 
Liquid blood-serum as a culture-medium, 
197 

Liquids of the tissues, • alterations of, 

cause edema, 62 
Lithopedion, 669 
Liver, 538 
abscess of, 546 

acute yellow atrophy of, 544 

adenoma of, 554 

amyloid degeneration of, 545 

anatomic considerations, 538 

anemia of, 539 

angioma of, 553 

atrophy of, 541 

localized, 542 
carcinoma of, 554 

secondary, 555 
changes of position of, 538 
circulatory disturbances of, 539 
cirrhosis of, 547 

atrophic, 548 

biliary, 550 

hypertrophic, 549 

Laennec's, 548 
cloudy swelling of, 543 
complete absence of, 538 
cyanotic induration of, 539 
cysts of, 556 

dropsical infiltration of, 545 
embolism of, 540 
fatty degeneration of, 543 
fatty infiltration of, 542 
fibromata of, 553 
gin-drinkers', 548 
hyperemia of, 539 
hypertrophy of, 551 
infectious diseases of, 551 
inflammations of, 546 
leprosy of, 553 
lipomata of, 553 



856 



INDEX. 



Liver, lymphadenoma of, 553 
malformations of, 538 
niyomata of, 553 
nutmeg-, 539 
parasites of, 556 

parenchymatous degeneration of, 543 

pigmentation of. 542 

red atrophy of, 539 

relation of, to diabetes, 41 

rupture of, 551 

sarcoma of, 553 

syphilis of, 552 

thrombosis of, 540 

tuberculosis of, 551 

tumors of, 553 
Liver-fluke, 308 
Livores mortis, 101 

Lobar pneumonia, 441. See Pneumonia. 

sclerosis of brain, 781 
Lobular pneumonia, 446 
Local anemia, 49 

hyperemia, 48 
Locomotor ataxia, 817 
Loffler's blood-serum, 198 

methylene-blue, 194 
Lophotrichous bacteria, 192 
Ludwig's angina, 493, 498 
Lungs, actinomycosis of, 472 

active hyperemia of, 431 

anatomic considerations, 430 

anemia of, 431 

atrophy of, 435 

carcinoma of, 474 

collateral hyperemia of, 431 

congenital defects of, 431 

congestion of, 431 

cyanotic induration of, 433 

cysts of, 475 

edema of, 433 

embolism of, 435 

emphysema of, 435 

gangrene of, 458 

glanders of, 472 

hemorrhage of, 433 

hemorrhagic infarcts of, 434 

hypertrophy of, 435 

hypostatic congestion of, 432 

inflammation of, 441 

parasites of, 475 

passive hyperemia of, 432 

sarcoma of, 473 

syphilis of, 470 

tuberculosis of, 459 

tumors of, 473 
Lupus vulgaris, 243 
Lustgarten's bacillus, 266 
Luxation of joints, 718 
Lymph adenia ossea, 717 

pauiciosa, 334 
Lymphadenitis, 350 

acute, 350 

chronic, 351 

suppurative, 350 
Lymphadenoma, 142, 346, 355 

aleukemic, 145 

appearance and seats of, 142 

etiology of, 142 



Lymphadenoma, leukemic, 145 
nature of, 144 
of liver, 553 
of mouth, 490 
structure of, 144 
Lymphangiectasia, 415 

acquired, 416 
Lymphangioma, 139 
cavernosum, 139 
of brain, 794 
of mouth, 490 
of spleen, 347 
Lymphangitis, 415 

purulent, 458 
Lymphatic anemia, 144 
circulation, obstruction of, a cause of 

edema, 63 
glands, amyloid degeneration of, 348 

anatomic considerations, 348 

anthracosis of, 350 

atrophy of, 348 

calcification of, 349 

carcinoma of, 357 

diseases of, 349 

fatty infiltration of, 348 

hyaline degeneration of, 349 

hypertrophy of, 348 

inflammation of, 350 

necrosis of, 349 

pigmentation of, 349 

sarcoma of, 357 

syphilis of, 355 

tuberculosis of, 352 

tumors of, 355 
leukemia, 336 

vessels, anatomic considerations, 415 
dilatation of, 415 
inflammation of, 415 
parasites of, 417 
syphilis of, 416 
tuberculosis of, 416 
tumors of, 416 
Lymphemia, 335 
Lymph-formation, causes of, 61 
Lymphocytes, 313 
Lymphogenic tuberculosis, 469 
Lymphoid infiltration, 144 

tubercle, 239 
Lymphoma, 142 
malignant, 142 
Lymphomatous infiltration of kidney, 610 
Lymph orrhea, 139 
Lymphosarcoma, 142, 150, 346, 355 
of mouth, 490 
of pituitary body, 797 
of stomach, 510 
of thymus gland, 359 

Mackocephaly, 749 

Macrocheilia, 139, 416, 490 

Macroglossia, 139, 416, 490 

Madura-foot, 261 

Malaria, hematozoon of, 282 
irregular, parasite of, 283 
relations of mosquitoes to, 284 

Malarial hematozoa, 282 
parasites, 282 



INDEX. 



857 



Malarial parasites, staining of, 340 
Male breast, abnormal development of, 
694 

Malignant edema, 251 

bacillus of, 251 
endocarditis, 368 
lymphoma, 142 
pustule, 252 
Mallein, 250 
Malta fever, 276 

micrococcus of, 276 
Malum coxa; seuilis, 720 
Mamma. See Mammary gland. 
Mammary gland, 694 

adenoma of, 698 

atrophy of, 696 

carcinoma of, 698 

chondroma of, 698 

congenital abnormalities of, 694 

cysts of, 700 

fatty infiltration of, 696 

fibroma of, 697 

hemorrhages of, 695 

hyperemia of, 694 

hypertrophy of, 696 

inflammation of, 695 

lipoma of, 697 

lipomatosis of, 696 

myoma of, 698 

myxoma of, 698 

myxomatous degeneration of, 696 

osteoma of, 698 

sarcoma of, 698 

supernumerarv, 694 

syphilis of, 696 

tuberculosis of, 696 

tumors of, 697 
Marantic thrombi, 57 
Margarin-crystals in fatty infiltration, 
70 

Marrow-cells, 357 

Massive cerebral hemorrhage, 769 

Mast-cell granules, 315 

Mast-cells, 314 

Mastitis, acute, 695 

chronic, 695 
Measles, animal parasites of, 290 

bacteriology of, 273 
Mechanical agents as causes of necrosis, 
93 

Meckel's diverticulum, 515 
Medicinal leukocytosis, 325 
Mediterranean fever, 276 
Medullary carcinoma, 179 

infiltration of lymphoid structures of 
intestine, 529 
Megaloblasts, 318 
Megalocytes, 317 
Megastoma entericum, 281 
Melsena neonatorum, 503 
Melanemia, 322 
Melanin, pigmentation by, 88 
Melanosarcoma, 152 
Melanuria, 626 

Membranes of brain, diseases of, 731 

of spinal cord, diseases of, 798 
Meningismus, 768 



Meningitis, epidemic cerebrospinal, 737 

tuberculous, 738 
Meningocele, 748 
Menorrhagia, 53, 642 
Menstruation, 641 
Mercury, poisoning by, 27 
Mesarteritis, 399 
Mesencephalon, 743 
Mesophilic bacteria, 196 
Metabolic pigmentation, 91 
Metabolism, disorders of, 32 

in diabetes, 41 
Metachromatic bodies, 191 
Metaplasia, 120 
Metastasis, 57 

Metastatic abscesses, production of, 56 
Methemoglobin in urine, 631 
Metritis, 642 

acute, 645 

chronic, 646 
Metrorrhagia, 53, 642 
Metschnikow's theory of phagocytosis 
206 

Miasmatic disease, definition of, 32 
Microblasts, 318 
Microcephaly, 749 
Micrococcus, 190 

exanthematicus, 274 

Maltensis, 276 

tetragenus, 214 

urea; in urine, 628 
Microcytes, 317 
Micromyelia, 804 
Microspira, 190 

Migula's classification of bacteria, 190 
Miliary aneurysm, 406 
of brain, 765 
of spinal cord, 809 

tubercles, 237, 242 
Milk as a culture-medium, 197 
Milk-spots, 394 
Miners' elbow, 724 
Mixed tumors, 136, 156 
Moist gangrene, 98 
Moles, flesh v, 674 

hydatid, 676 
Molluscum contagiosum, animal parasites 

of, 289 
Molluscum-bodies, 289 
Mononuclear leukocytes, 313 
Monostoma lentis, 310 
Monotrichous bacteria, 192 
Morbid anatomy, definition of, 17 
Morbus cseruleus, 362 
Morphin, poisoning by, 30 
Mosquitoes, relations of, to malaria, 284 
Mother-wreath, 117 
Mouth, anemia of, 484 

circulatory disturbances of, 484 

congenital abnormalities of, 484 

hemor images of, 484 

hyperemia of, 484 

inflammation of, 484 

syphilis of, 489 

tuberculosis of, 488 

tumors of, 490 
Movable spleen, 341 



858 



INDEX. 



Mucin, hypersecretion of, distinguished 
from mucoid degeneration, 79 
nature of, 79 
staining of, 80 
Mucoid degeneration, 79. See Degenera- 
tion. 

of bone-marrow, 357 
Mucopurulent catarrh, 111 

cystitis, 619 
Mucous colitis, 526 

patch, 267, 269 
Mulberry calculi, 621 
Multiple sclerosis of brain, 781 
Multipolar karyokinesis, 100 
Mumps, 498 

bacteriology of, 273 
Mural endocarditis, 366 

fibroids, 650 
Muscarin, poisoning by, 30 
Muscles, actinomycosis of, 730 

amyloid degeneration of, 729 

anemia of, 725 

anthrax of, 730 

atrophy and degeneration of, 727 

calcification of, 729 

carcinoma of, 731 

chondroma of, 730 

coagulation-necrosis of, 729 

congenital malformations, 724 

diseases of, 724 

embolism of, 725 

fatty degeneration of, 729 

fatty infiltration of, 729 

fibromata of, 730 

glanders of, 730 

hemorrhages of, 725 

hyaline degeneration of, 729 

hyperemia of, 725 

hypertrophy of, 724 

inflammation of, 725. See Myositis. 

lipomata of, 730 

myxomata of, 730 

osteoma of, 730 

parasitic diseases of, 731 

parenchymatous degeneration of, 729 

rhabdomyomata of, 730 

sarcoma of, 730 

syphilis of, 730 

thrombosis of, 725 

tuberculosis of, 730 

tumors of, 730 
Muscular atrophy, myopathic, 728 
neuropathic, 727 
progressive, 728 
pseudohypertrophic, 729 
simple, 729 
Mycetoma, 261 
Mycophylaxins, 209 
Mycoprotein, 193 
Mycosis aspergillina, 429 

fungoides, 156 
Mycosozins, 209 
Mycotic endocarditis, 368 
Mydalein, poisoning by, 30 
Mydatoxin, poisoning by, 30 
Myelinic neuroma, 161 
Myelitis, 811 



Myelitis, hematogenous purulent, 812 
pressure-, 814 

secondary to purulent leptomeningitis, 
812 

transverse, secondary to injury or in- 
fectious disease, 812 
Myelocytes, 314 
Myelogenous callus, 704 

osteosarcoma, 155 
Myeloid sarcoma, 154 
Myeloma, 145, 717 
Myelomeningocele, 805 
Myiasis, 311 

Myocardite segmentaire, 378 
Myocarditis, 379 

acute, 379 

circumscribed, 379 
diffuse, 380 

chronic, 382 
Myofibroma of ovary, 658 

of uterus, 650 

of vagina, 672 

of vulva, 678 
Myoma cavernosum, 162 

cysticum, 162 

lsevicellulare, 161 

of bladder, 623 

of liver, 553 

of mammary gland, 698 

of stomach, 510 

of uterus, 162 

striocellulare, 164 
Myomalacia, 390 

cordis, 365 
Myoneuroma of pituitary body, 797 
Myopathic muscular atrophy, 728 
Myositis, 725 

chronic, 726 
productive, 727 
suppurative, 726 

disseminated acute, 726 

hemorrhagic, 725 

localized acute, 725 

ossificans progressiva, 727 

ossifying, 727 

serous, 725 

suppurative, 726 
Myxedema, 581 

Myxoid cystomata of ovaries, 658 
Myxoma, 130 

appearance of, 131 

definition of, 130 

etiology, 131 

nature of, 132 

of bladder, 623 

of bone, 716 

of dura mater of cord, 800 
of intestines, 533 535 
of mammary gland, 698 
of mouth, 490 
of muscles, 730 
of testicle, 687 
seats of, 131 
structure of, 131 
Myxomatous degeneration of mammary 
gland, 696 
of testicle, 682 



INDEX. 



859 



N^vus lyinphaticus, 139 

promiuens, 140 
Nasal catarrh, acute, 418 

cavities, active congestion of, 418 

anatomic considerations, 418 

congenital abnormalities of, 418 

edema of, 418 

hemorrhage of, 418 

inflammations of, 418 

parasites of, 420 

passive congestion of, 418 

syphilis of, 419 

tuberculosis of, 419 

tumors of, 419 
Natural immunity, 205 
Necrobiosis, 91 
Necrosis, 91 
cellular, general pathology of, 100 
coagulation-, 93 
definition of, 91 
etiology of, 92 
fat-. 97 

of pancreas, 564 
liquefaction-, 95 
of bone, 711 

of lymphatic glands, 349 
of pancreas, 564 
Necrotic appendicitis, 524 

inflammation, 115 
Negative chemotaxis, 104 
Neisser, gonococcus of, 215 
Neisser's method of staining diphtheria 

bacilli, 222 
Nematodes, 300 
Neoplasms, 121. See Tumors. 
Nephritis, 588, 591 
acute catarrhal, 590 
degenerative, 590 
desquamative, 590 
diffuse, 591 
hemorrhagic, 591 
inflammatory lesions from, 602 
interstitial, 591 
parenchymatous, 590 
arteriosclerosis from, 602 
arteriosclerotic, 596 
cardiac changes from, 602 
chronic, 593 

hemorrhagic, 593 
interstitial, 595 
diffuse, 589 

edema or dropsy from, 603 
embolic suppurative, 592 
etiologv of, 589 
gouty, 596 
interstitial, 589 
parenchymatous, 589 

chronic, 593 
pathologic anatomy of, 589 

physiology of, 598 
results of, 602 
secondary interstitial, 594 
suppurative, 592 
tube-casts in, 599 
uremia from, 603 
urine in, 599 
Nerve-cell, anatomy of, 752 



Nerve-cell, changes in nuclei of, 756 
degenerative changes in, as a whole, 
757 

degenerative processes of, 752 

functions of, 758 

Nissl's method of staining, 753 

pathologic changes in, 752 

pigmentation of, 756 

vacuolization of, 755 
Nerve-fibers, anatomy of, 758 

degeneration of, 759 

functions of, 759 
Nerve-poisons, 30 
Nerves, 828 

atrophy of, 828 

degeneration of, 829 

edema of, 828 

hemorrhages into, 828 

hyperemia of, 828 

inflammation of, 831. See also Neur- 
itis. 

leprosy of, 834 

muscular fibers in, 834 

regeneration of, 829 

sarcoma of, 834 

syphilis of, 833 

tuberculosis of, 833 

tumors of, 834 
Nervous system, central, injuries of, 783 
general pathologic anatomy of, 752 
influence of, in causation of edema, 
63 

Neurin, poisoning by, 30 
Neuritis, 831 

acute interstitial, 831 

chronic hypertrophic interstitial, 833 

chronic interstitial, 832 

parenchymatous, 833 

suppurative, 833 
Neuroblasts, 743 
Neuroglia, degeneration of, 760 
Neurcglioma, ganglionar, 786 
Neuroma, 161 

amyelinic, 161 

false, 161 

myelinic, 161 

of suprarenal bodies, 584 

plexiform, 161 

true, 161 
Neuron, description of, 746 
Neuroparalytic hyperemia, 48 
Neuropathic arthritis, 721 

hemorrhage, 52 

muscular atrophy, 727 
Neurotic hyperemia, 48 
Neuropil iles, 314 
Neutrophilic granules, 315 
New-growths, 121. See also Tumors. 
Nigrities of tongue, 488 
Nissl's method of staining nerve-cells, 
753 

Nitrate of silver, poisoning by, 25 
Nitric acid, poisoning by, 25 
Nitrifying ferments, 200 
Nitrobenzol, poisoning by, 29 
Nitroglycerin, poisoning by, 29 
Nodes of Eanvier, 759 



860 



INDEX. 



Noma, 486 

Non-contagious disease, definition of, 31 
Non-siderous pigments, 88 
Normoblasts, 318 

Nourishment, insufficient, effect of, 33 

Nuclear solution, 100 

Nuclei of cells, degenerations of, 100 

of nerve-cells, morbid changes in, 756 
Nucleo-albuminuria, 629 
Numerical atrophy, 65 

hypertrophy, 121 
Nutmeg- liver, 539 
Nutrition, disorders of, 32 

Obesitas cordis, 375 
Obesity, 33 

associated conditions, 34 

causes of, 34 

pathologic anatomy of, 34 
Obligate saprophytes and parasites, 196 
Obstruction, intestinal, 517 

of bronchi, 428 
Obstructive thrombus, 59 
Odontinoids, 491 
Odontoma, 138, 491 
OSdema ex vacuo, 62 
Oid i urn albicans, 265, 488 
Oligemia, 321 
Oligochromemia, 327 
Oligocythemia, 327 
Omentum, dropsy of, 569 
Oophoritis, 657 

chronic, 657 
Optic thalami, 745 
Orchitis, 682 

acute, 683 

chronic, 683 
Organic poisons, 26 
Ose, 198 

Osmosis, escape of fluid by, 61 
Ossification, 86 

differentiation of, from calcification. 

86 

Ossifying myositis, 727 

pachymeningitis, 732 

periostitis, 707 
Osteitis, 707 

chronic, 708 

condensing, 709 
Osteo-arthropathy. hypertrophic, 707 
Osteochondroma, 136 
Osteoclasts, 709 
Osteoid chondroma, 136 

sarcoma, 717 
Osteoma, 137 

appearance of, 137 

definition of, 137 

dental, 138 

durum, 138 

eburneum, 138 

etiology of, 137 

heteroplastic, 138 

nature of, 139 

of brain, 794 

of lungs, 473 

of mammary gland, 698 

of muscles, 730 



Osteoma of pleura, 482 

of testicle, 687 

seats of, 138 

spongiosum, 138 

structure of, 138 
Osteomalacia, 711 
Osteomyelitis, 358, 707 
Osteophytes, 137 
Osteoporosis, inflammatory, 709 
Osteopsathyrosis, 710 
Osteosarcoma, 154 

myeloid, 155 
Osteosclerosis, 709 
Ovaries, 655 

absence of, 656 

active hyperemia of, 656 

adenocystoma of, 658 

carcinomata of, 661 

chondromata of, 658 

congenital abnormalities of, 656 

congestion of, 656 

cysto-adenoma of, 658 

cystoma of, papillary, 659 

cystomata of, colloid, 658 
glandular, 658 
myxoid, 658 

dermoid cysts of, 660 

development and anatomic considera- 
tions, 655 

dislocation of, 656 

fibroma of, 658 

fibrosarcomata of, 658 

follicular cysts of, 658 

hemorrhages into, 656 

hypoplasia of, 656 

inflammation of, 657 

myofibromata of, 658 

passive congestion of, 656 

sarcoma of, 658 

supernumerary, 656 

tuberculosis of, 657 

tumors of, 658 
Overaction of heart, effect of, on circula- 
tion, 47 
Overfeeding, effect of, 33 
Oviducts. See Fallopian tubes. 
Oxalate of lime in urine, 629 
Oxalic acid, poisoning by, 25 
Oxaluria, 42 
Oxidizing ferments, 200 
Oxyphile granules, 314 
Oxyuris vermicularis, 301, 537 
Ozena, 419 

Ozeena syphilitica, 419 

Pacchionian bodies, 740 
Pachydermia laryngis, 421 
Pachymeningitis, 731 
cervicalis, 799 

external tuberculous, of cord, 799 
hemorrhagic, 731 

internal hemorrhagic, of cord, 799 
ossifying, 732 
productive, 732 
suppurative, 732 
Pancreas, 563 
amyloid degeneration of, 564 



INDEX. 



861 



Pancreas, atrophy of, 563 
carcinoma of. 566 
circulatory disturbances of, 563 
cirrhosis of, 565 

congenital abnormalities of, 563 
cysts of, 566 
fat-necrosis of, 564 
hematochromatosis of, 564 
hemorrhage in, 563 
hyperemia of, 563 
inflammation of, 565 
necrosis of, 564 

parenchymatous degeneration of, 564 

pigmentation of, 564 

relation of, to diabetes, 41 

sarcoma of, 566 

syphilis of, 566 

tuberculosis of, 566 

tumors of, 566 
Pancreatic calculi, 567 

duct, 567 

dilatation of, 567 
obstruction of, 567 

veins, 567 
Pancreatitis, 565 

acute hemorrhagic, 565 
suppurative, 565 

chronic indurative, 565 

necrotic, 565 
Pandemic disease, 31 
Papillary cystoma of ovary, 659 

tumors, 125 
Papuliferous cystic adenoma of kidney, 
610 

cystoma of testicle, 688 
cystomata, 185 
Papilloma, 164 
hard, 165 
of bladder, 622 
of Fallopian tubes, 667 
of intestines, 533 
of larynx, 423 
of mouth, 490 
of penis, 680 
of vagina, 672 
soft, 165 

Papillomatous tumors of vulva, 678 
Parachromophoric bacteria, 203 
Paradoxic embolism, 54 
Paralysis, general progressive, 780 
Paramecium coli, 280 
Parametritis, 642 
Parapbimosis, 679 
Parasites, 195 

animal, 277 

embolism by, 54 

in etiology of disease, 32 

of blood, 338 

of bone, 717 

of bronchi, 429 

of heart, 391 

of intestine, 536 

of kidney, 612 

of larynx, 424 

of liver, 556 

of lungs, 475 

of lymphatic vessels, 417 



Parasites of nasal cavities, 420 

of pericardium, 396 

of peritoneum, 575 

of pleura, 483 

of spleen, 347 

of thyroid gland, 580 

of ureter, 616 

of uterus, 655 

vegetable, 30 
Parasitic disease, definition of, 32 

stomatitis, 488 

theory as to origin of carcinoma, 171 
Parenchyma-poisons, 26 
Parenchymatous encephalitis, 776 

glossitis, 487 

goiter, 577 

degeneration, 66. See Cloudy swelling. 

of heart, 374 

of kidnev, 604 

of liver, 543 

of muscles, 729 

of pancreas, 564 
hemorrhage, 50 
hepatitis, 546 
inflammation, 112 
nephritis, 589 

acute, 590 

chronic, 593 
neuritis, 833 

tissue, regeneration of, 119 
Paroophoron, 656 
Parotitis, 498 
Parovarium, 656 

cysts of, 661 
Paroxysmal hemoglobinuria, 627 
Passive hyperemia, 48 

immunity, 205 
Pathologic anatomy, definition of, 17 

chemistry, definition of, 17 
Pathology, definition of, 17 

general, 17 

special, 312 
Patulous ductus Botalli, 362 
Pearl disease, 240 
Pelvis of kidney, 613 
calculus in, 614 
inflammation of, 614 
malformations of, 613 
tuberculosis of, 615 
tumors of, 616 
Penis, 679 

angioma of, 681 

carcinoma of, 680 

condyloma acuminatum, 680 

congenital abnormalities of, 679 

cysts of, 680 

epithelioma of, 680 

fibroma of, 681 

inflammation of, 679 

injuries of, 681 

lipoma of, 681 

papilloma of, 680 

tuberculosis of, 680 

tumors of, 680 
Pentastomum denticulatum, 311, 557 

ttenioides, 311 
Peptic ulcer of intestine, 522 



862 



INDEX. 



Peptic ulcer of stomach, 506 
Peptone, formation of, 36 

poisoning by, 30 

solution, 199 
Peptonuria, 37 
Perforative peritonitis, 571 
Periangiocolitis, 551 
Periarteritis, 499 

nodosa, 400 
Peribronchial fibrous pneumonia, 455 
Peribronchitis, 428 
Pericarditis, 392 

associated conditions of, 395 

dry, 392 

fibrinous, 392 

hemorrhagic, 394 

interna et externa, 396 

purulent, 394 

serofibrinous, 393 

terminations of, 394 
Pericardium, 360, 391, 394 

actinomycosis of, 396 

hemorrhages in, 392 

hyperemia of, 392 

inflammation of, 392 

parasites of, 396 

syphilis of, 396 

tuberculosis of, 396 

tumors of, 396 
Perichondritis of larynx, 421 
Perihepatitis, 551 

hyperplastic, 573 
Perilymphangitis, 458 
Perimastitis, 695 
Perimetritis, 642 
Perinephritis, 588 
Peri-orchitis, 684 

prolifera, 684 
Periosteal callus, 704 
Periostitis, 706 

ossifying, 707 

purulent, 707 

simple, 706 

syphilitic, 715 
Peripheral nervous system, 827 
Periproctitis, 527 
Periprostatitis, 689 
Perisplenitis cartilaginea, 345 
Perithelioma, 793 
Peritoneum, 568 

carcinoma of, 574 

circulatory disturbances of, 568 

congenital abnormalities of, 568 

dropsy of, 569 

echinococcus cysts of, 575 

fibromata of, 574 

hemorrhage of, 568 

hyperemia of, 568 

inflammation of, 570. See Peritonitis. 
lipomata of, 574 
parasites of, 575 
sarcoma of, 574 
tuberculosis of, 573 
tumors of, 574 
Peritonitis, 570 
acute general, 572 
localized, 571 



Peritonitis, chronic, 572 

hemorrhagic, 572 

idiopathic, 570 

micro-organisms of, 571 

perforative, 571 
Peritrichous bacteria, 192 
Perityphlitic abscess, 525 
Perityphlitis, 525 
Periurethral abscess, 633 
Perivascular fibrous pneumonia, 455 
Pes calcaneus, 718 

equinus, 718 

valgus, 718 

varus, 718 
Petechia, definition of, 53 
Petri's dishes, 198 
Phagedenic ulcer, 111 

ulceration of cervix uteri, 645 
Phagocytes, 206 
Phagocytosis, 206 
Pharyngitis, catarrhal, 492 

chronic catarrhal, 492 

phlegmonous, 493 

pseudomembranous, 493 
Pharyngomycpsis leptothricia, 265, 497 
Pharynx, anemia of, 492 

diphtheria of, 496 

edema of, 492 

glanders of, 497 

hemorrhages of, 492 

hyperemia of, 492 

inflammation of, 492 

lepra of, 497 

pressure-necrosis of, 495 

syphilis of, 497 

tuberculosis of, 497 

tumors of, 497' 
Phimosis, 679 
Phlebectasia, 413 
Phlebectatic elephantiasis, 414 
Phlebitis, 412 

acute, 412 

chronic, 412 
Phleboliths, 61, 412 
Phlebosclerosis, 412 
Phlegmonous cystitis, 619 

esophagitis, 500 

inflammation of vulva, 677 

pharyngitis, 493 

stomatitis, 486 

tonsillitis, 494, 495 
Phlogogenic bacterial proteins, 199 
Phloridzin-glycosuria, 39 
Phosphates in urine, 629 
Phosphatic calculi, 621 
Phosphaturia, 42 

Phosphoric acid, excessive formation of, 

in body, 36, 41 
Phosphorus, poisonous action of, 26 
Photogenesis, 203 
Phragmodiothrix, 190 
Phthisis, fibroid, 265 
Phylaxins, 209 
Physometra, 640 
Pia mater, cerebral, 734 

anemia of, 734 

cholesteatomata of, 741 



INDEX. 



863 



Pi a mater, cerebral, edema of, 734 

endothelioma of, 740 

hemorrhages of, 734 

hyperemia of, 734 

inflammation of, 735 

lipoma of, 741 

syphilis of, 740 

teratomata of, 742 
spinal, 806 

calcareous infiltration of, 800 

hyperemia of, 800 

inflammation of, 800 

syphilis of, 801 

tuherculosis of, 801 
Pigment-building cells, 91 
Pignient-metastases, 89 
Pigmentation, 86 

by cutaneous absorption, 88 

by foreign bodies, 86 

by hemoglobin-derivatives, 88 

by salts of silver, 87 

from the exterior, 86 

hematogenous, 88 

hepatogenous, 90 

metabolic, 91 

of bone-marrow, 357 

of choroid plexus, 790 

of intestines, 519 

of liver, 542 

of lymphatic glands, 349 
of mucosa of stomach, 508 
of nerve-cell, 756 
of pancreas, 564 
of red blood-corpuscle, 319 
of spinal pia, 800 
of spleen, 346 
of suprarenal bodies, 583 
Pigmented sarcoma, 153 
Pineal gland, 745, 798 
Pin -worm, 301 
Pituitary body, 794 

adenoma of, 797 

amyloid degeneration of, 796 

colloid degeneration of, 796 

cysts of, 797 

hemorrhage into, 796 

hyperemia of, 796 

hypertrophy of, 795 

inflammation of, 796 

lymphosarcoma of, 797 

relation of, to acromegaly, 797 

sarcoma of, 797 

softening of, 796 

syphilis of, 796 

tuberculosis of, 796 

tumors of, 796 
Placenta, 672 

abnormal development of, 673 
hemorrhage into, 674 
inflammation of, 674 
prsevia, 673 
succenturiata, 673 
syphilis of, 675 
tuberculosis of, 675 
Placental infarcts, 674 

polyps, 675 
Placentitis, 674 



Planococcus, 190 
Planosarcina, 190 
Plaques jaunes, 775 
Plasma of blood, 398 
Plasma-cells, 104 
Plasmodia, 282 
Plehn's solution, 340 
Plethora, 320 

apocoptica, 321 

hydremica, 321 

vera, 320 
Pleura, 476 

circulatory disturbances of, 476 

inflammation of, 477 

parasites of, 483 

passive hyperemia of, 476 

petechial hemorrhages of, 476 

syphilis of, 482 

tuberculosis of, 481 

tumors of, 482 
Pleurisy, 477. See Pleuritis. 

bread-and-butter, 479 
Pleuritis, 477 

fibrinous, 478 

hemorrhagic, 480 

purulent, 479 

serofibrinous, 479 
Pleurogenic fibrous pneumonia, 455 

pneumonia, 441 

purulent pneumonia, 458 
Plexiform angiosarcoma, 151 

neuroma, 161 
Pneumaturia, 626 
Pneumonia, 441 

alba, 456, 470 

aspiration-, 447, 450 

catarrhal, 446 
bacteria of, 219 

cheesy, 451 

congenital syphilitic, 456 
croupous, 441. See Pneumonia, fibrin- 
ous. 

bacteriology of, 216 
deglutition-, 447 
desiccans, 458 
fibrinous, 441 

associated lesions in, 445 

etiology of, 441 

pathologic anatomy of, 442 
physiology of, 445 

stage of congestion or engorgement, 
442 

of consolidation or hepatization, 
443 

of resolution in, 444 

usual characters of, 444 

usual terminations of, 445 
fibrous, 453 

peribronchial, 455 

perivascular, 455 

pleurogenic, 455 

secondary, 455 
hematogenic, 441 
hypostatic, 447, 450 
irregular, 219 

lobar, 441. See Pneumonia, fibrinous. 
lobular, 446 



864 



INDEX. 



Pneumonia, migrans, 442 

pleurogenic, 441 

productive, 453 

purulent, 456 

bronchogenic, 456 
hematogenic, 457 
pleurogenic, 458 

tubercular, 219 

tuberculous, 451 
Pneumonic tuberculosis, 461 
Pueumonokoniosis, 86, 453 
Pneumonomycosis aspergillina, 245, 476 
Pneumopericardium, 396 
Pneuniopyopericardiuin, 397 
Pneumothorax, 477 
Poikilocytosis, 318 
Poisous, action of, in general, 24 

blood-, 29 

classification of, 25 

corrosive, 25 

effect of, 24 

elimination of, 25 

fate of, after ingestion, 24 

immunity to, 24 

in etiology of disease, 24 

necrosis from, 92 

nerve-, 30 

organic, 28 

parenchyma-. 28 
Polar spore, 191 

field, 117 
Poliomyelitis, acute anterior, 815 

chronic anterior, 823 
Polycholia, 562 
Polychromatophilia, 319 
Polycythemia, 324 
Polymastia, 694 

Polymorphonuclear leukocytes, 314 
Polymorphous heredity, 38 
Polymyositis, 726 

secondary acute, 729 
Polyneuritis, 833 
Polynuclear leukocytes, 314 
Polypoid elevations of stomach, 510 

growths of bladder, 622 

outgrowths from tooth-pulp, 491 

tumors, 125 
Polyps, nasal, 419 

placental, 675 

of uterus, 650 
sarcomatous, 652 
Polyuria, 624 
Pons, anatomy of, 745 
Porencephaly, 762 

Portal vein, embolism and thrombosis 

of, 540 
Port-wine stains, 140 
Posterior sclerosis of spinal cord, 817 
Posthitis, 679 

Post-mortem alterations, 100 

circulatory phenomena, 100 

degeneration of tissues, 101 

lividity, 46 
Potassium chlorate, poisoning by, 29 
Potato-extract, 197 
Predisposing causes of disease, 18 
Predisposition to disease, 18 



Pregnancy, abdominal, 670 

extra-uterine, 668 

interstitial, 668 

tubal, 668 
Prepuce, concretions under, 681 

inflammation of, 679 
Pressure, effect of, on tissues, 19 
Pressure-myelitis, 814 
Pressure-necrosis of pharynx, 495 
Primary anemias, 329 

gangrene, 98 

thrombus, 59 
Processes of nerve-cell, degenerative 

changes in, 752 
Proctitis, 526 

Productive inflammation, 111 

myositis, chronic, 727 

pachymeningitis, 732 

pneumonia, 453 
Proglottides of tape-worms, 291 
Progressive muscular atrophy, 728 

pernicious anemia, 331 

spinal muscular atrophy, 823 

tissue-changes, 120 
Projection-fibers of brain, 744 
Prolapse of rectum, 519 

of uterus, 638 

of vaginal walls, 670 
Proliferation-cysts, 184 
Proliferative cystomata, 185 
Prosencephalon, 743 
Prostate gland, 689 

abscess of, 689 

atrophy of, 690 

carcinoma of, 693 

concretions in, 690 

cysts of, 693 

fatty degeneration of, 690 

hypertrophy of. 690 

inflammation of, 689 

sarcoma of, 693 

tuberculosis of, 690 
Prostatitis, 689 

phlegmonous, 689 

simple, 689 

suppurative, 689 
Proteins produced by bacteria, 199 
Proteolytic ferments, 200 
Proteus infection, 274 
Protozoa, 277 
Psammoma, 85, 156, 794 
Psammoma-bodies, 84, 659 
Pseudarthroses, 705 
Pseudodichotomy of bacteria, 193 
Pseudodiphtheria bacillus, 222 
Pseudohvpertrophic muscular atrophy, 
729 

Pseudoleukemia, 144, 337 

cutis, 157 

infantum, 337 
Pseudomembranous cystitis, 620 

enteritis, 522 

esophagitis, 499 

gastritis, 503 

pharyngitis, 493 

stomatitis, 486 

vaginitis, 671 



INDEX. 



865 



Pseud omonas, 190 
Pseudomucin, 80 
Pseudoplasms, 121. See Tumors. 
Pseudotrichinosis, 726 
Pseudotuberculosis, 244 
Psorosperrnise, 285 
in liver, 556 

in pelvis of kidney, 616 
Psychrophilic bacteria, 196 
Ptomains, poisoning by, 30 
Puerperal infections of uterus, 646 
etiology of, 646 
pathologic anatomy of, 647 
Pulmonary artery, stenosis and atresia 
of, 361 

infarcts, 57 
Pulsion-diverticula of esophagus, 500 
Punctate cerebral hemorrhage, 769 
Purulent arthritis, 720 

lymphangitis, 458 

myelitis, hematogenous, 812 

pericarditis, 391 

periostitis, 707 

pleuritis, 479 

pneumonia, 456 

vaginitis testis, 685 
Pustule, malignant, 252 
Putrefaction, 200 
Pyelitis, 588, 614 
Pyelonephritis, 615 

suppurative, 592 
Pyemia, 204 

Pyknomorphous state, 755 
Pvknosis, 100 
Pylephlebitis, 541 
Pyogenic albumosuria, 626 

bacterial proteins, 199 

membraiie, 111 
Pyoid marrow, 358 
Pyonephrosis, 615 
Pyorrhoea alveolaris, 486 
Pyosalpinx, 666 
Pyothorax, 479 

Pyramidal tract, degeneration of, 772 
Pyrosoma bigeminum, 285 

Quartan malaria, organism of, 283 
Quinsy, 495 

Rabies, bacteriology of, 274 
Eacemose adenoma, 167 

cystieerci, 293 
Rachitic rosary, 702 
Rachitis, 701 
Ranula, 490 
Ranulse, 184 
Ray fungus, 258 
Rectocele, 639 

vaginal, 670 
Rectum, inflammation of, 526 

prolapse of, 519 
Recurrent fibroid tumor, 148 
Recurring appendicitis, 526 
Red atrophy of liver, 539 

blood-corpuscles, 312. See Blood-cor- 
puscle. 
nucleated, 318 

55 



Red granular kidney, 596 

hepatization of lung, 443 

softening of brain, 774 
Reducible hernia, 517 
Regeneration, 116 

normal, 116, 117 

of bone, 703 

of connective tissues other than fibrous, 
119 

of fibrous connective tissues, 118 
of nerves, 829 

of parenchymatous tissue, 119 

pathologic, 117 
Relapsing appendicitis, 526 

fever, 262 
Relative immunity, 205 
Remote heredity, 18 
Renal calculi, 614 

"rests," 582 

sand, 614 
Repair of wounds, 112 
Reproductive organs, diseases of, 636 
Resolution after inflammation, 115 
Respiratory system, diseases of, 418 
Retention-cysts, 184 
Retroflexion of uterus, 638 
Retrograde embolism, 54 
Retrogressive processes, 64 
Retroperitoneal hernia, 516 
Retropharyngeal abscess, 493 
Retro-uterine hematocele, 642 
Rhabdomyoma, 164 

of muscles, 730 

of testicle, 687 
Rhabdomyosarcoma of kidney, 609 
Rhachischisis, 748 
Rheumatism, bacteriology of, 275 
Rheumatoid arthritis, 720 
Rhinitis, acute, 418 

atrophica, 419 

chronic, 419 

diphtheritic. 419 
Rhinoliths, 420 
Rhinoscleroma, 219 

affections of nasal cavities in, 419 
Rhopalocephalus carcinomatosus, 288 
Rice-water stools of cholera, 528 
Ricin, poisoning by, 28 
Rickets, 701 

congenital, 703 
Rigor mortis, 100 
Round ulcer of stomach, 506 

worms, 300 
Round-cell infiltration, 104 
Round-celled sarcoma, 149 
Rubeola, 273. See Measles. 
Rupture of bladder, 618 

of intestines, 537 

of liver, 551 

of uterus, 641 

Saccular aneurysm, 407 

bronchiectasis, 429 
Sago spleen, 346 

Salivary ducts, concretions in, 499 
cystic dilatation of, 499 
diseases of, 498 



866 



INDEX. 



Salivary fistulse, 498 

glands, inflammation of, 498 
tumors of, 498 
Salpingitis, 664 

acute, 664 

chronic, 666 

diphtheritic, 665 
Sanarelli's bacillus, 272 
Sapremia, 204 
Saprophytes, 195 
Sarcina, 190 
Sarcinse veutriculi, 510 
Sarcolactic acid, excessive formation of, 

in body, 36 
Sarcoma, 145 

alveolar, 150 

appearances of, 146 

blood-vessels of, 147 

giant-celled, 154 

myeloid, 154 

of bone, 716 

of brain, 786 

of cervix uteri, 652 

of dura mater of cord, 800 

of Fallopian tubes, 668 

of intestines, 533 

of kidney, 609 

of liver, 553 

of lungs, 473 

of lymphatic glands, 357 

of mammarv gland, 698 

of mouth, 490 

of muscles, 730 

of nerve, 834 

of ovaries, 658 

of pancreas, 566 

of peritoneum, 574 

of pituitary body, 797 

of pleura, 482 

of prostate, 693 

of spinal cord, 827 

of spleen, 347 

of stomach, 510 

of suprareual bodies, 584 

of testicle, 687 

of thymus gland, 359 

of thyroid gland, 580 

of tooth-pulp, 491 

of urethra, 636 

of uterus, 652 

of vagina, 672 

of vulva, 678 

osteoid, 217 

pigmented, 153 

round-celled, 149 

seats of, 147 

spindle-celled, 148 
Sarcomatosis, 147 
Sarcomatous cylindromata, 152 

polyps of uterus, 652 
Sarcosporidia, 286 
Sarkodina, 277 
Scarlatina. See Scarlet fever. 
Scarlet fever, animal parasites of, 290 

bacterium of, 273 
Scirrhous carcinoma, 179 
Sclerosis of brain, atrophic, 761 



Sclerosis of brain, diffuse, 760 
disseminated, 761 
hvpertrophic, 762 
lobar, 781 
multiple, 781 
of spinal cord, amyotrophic later 
822 

combined, 823 
posterior, 817 
Scolex of tape-worm, 291 
Scrofula, 353 
Scrotum, 679 

cysts of, 680 

elephantiasis of, 680 

epithelioma of, 680 
Seat- worm, 301 
Secondary anemia, 327 

gangrene, 98 

thrombus, 59 
Segmentation, indirect, 117 

of fibers of heart, 378 
Seminal vesicles, 693 

diseases of, 694 
Senile arthritis, 720 

atrophy of uterus, 649 

emphysema of lungs, 438 
Septicemia, 204 
Septic endocarditis, 368 
Sequestrum, 711 
Serofibrinous pericarditis, 393 

pleuritis, 479 
Serous arthritis, 720 

inflammation, 107 

myositis, 725 

vaginitis testis, 684 
Serpents, venom of, poisoning by, 28 
Serpiginous ulcer, 111 
Serum, " lysogenic " action of, 206 
Serum-reaction of Widal, 227 
Seruinuria, 626 
Shadow corpuscles, 319 
" Shaven-beard " appearance, 530 
Siderosis, 86, 455 
Siderous pigments, 88 
Silver-salts, pigmentation by, 86 
Slumbering cells of Grawitz, 106 
Smegma bacillus, 243 
Soft chancre, 271 

papilloma, 165 
Softening cysts, 184 
Sozins, 209 

Special pathology, 312 

definition of, 17 
Spermatocele, 688 
Sphacelinic acid, 28 
Sphacelus, 100 
Spina bifida, 804 
Spinal cord, 798 

abnormal smallness of, 804 

anatomy of, 802 

anemia of, 809 

aneurysms of, 809 

blood-vessels of, degeneration 
walls of, 808 

carcinoma of, 827 

cysts of, 827 

degenerations of, secondary, 825 



INDEX. 



867 



Spinal cord, development of, 742 
double, 804 
glioma of, 827 
hyperemia of, 809 
inflammations of, 811 
primary degenerations of, 817 
sarcoma of, 827 

sclerosis of, amyotrophic lateral, 822 
combined, 823 
posterior, 817 
total absence of, 804 
tumors of, 827 
unusual length of, 804 
varicose veins of, 810 
white matter of, degeneration of, 824 
ganglia, disease of, 828 
Spindle-celled sarcoma, 148 
Spindle-shaped aneurysm, 406 
Spirillacese, 190 
Spirillum, 190 
Berolinensis, 232 
cholerse Asiaticse. 229 

pathogenicity of, 230 
Metschnikowi, 232 
of Finkler and Prior, 232 
tyrogenicum, 232 
Spirochaeta, 190 

Obermeieri, 262 
Spirosoma, 190 
Splanchnoptosis, 509 

Spleen, abnormal development and situ- 
ation of, 341 
abscess of, 344 

amyloid degeneration of, 345 
anemia of, 342 
atrophy of, 345 
calcification of, 346 4 
carcinoma of, 347 
chronic hyperplasia of, 345 

inflammation of, 345 
circulatory disturbances in, 342 
congestion of, 342 
cysts of, 347 
embolism of, 342 
hemorrhages in, 342 
hyaline degeneration of, 346 
hyperemia of, 342 
infectious diseases of, 347 
inflammation of, 343 
movable, 341 

pathologic physiology of, 341 

pigmentation of, 346 

sarcoma of, 347 

syphilis of, 348 

thrombosis of, 343 

tuberculosis of, 347 

tumors of, 346 
Splenemia, 335 
Splenic anemia, 329 

fever, 252 

stones. 343 
Splenitis, 343 

circumscribed, 344 

diffuse, 343 

spodogenous, 346 
Splenization of lung-tissue, 433, 440 
Spodogenous splenitis, 346 



Spongioblasts, 742 
Spores of bacteria, 191 

staining of, 195 
Sporozoa, 277 

Squamous cancer of stomach, 514 

epithelioma, 178 
Staining of bacteria, 193-195 

of blood, 339 
Staphylococcus epidermidis albus, 212 

pyogenes albus, 212 
aureus, 211 
citreus, 212 
Starvation, 33 
Stasis of blood, 49 
Staubzellen, 453 
Stenosis of biliary ducts, 559 

of esophagus, 500 

of Fallopian tubes, 663 

of heart-valves, 371 

of intestines, 515 

of uterus, 640 

of vagina, 670 
Stercoral typhlitis, 523 
Stomach, adenocarcinoma of, 514 

adenomatous proliferation of glands of, 
511 

alteration in position of, 509 
amyloid degeneration of submucosa of, 
509 

anemia of, 502 
anthrax of, 510 
atrophy of, 508 

calcification of mucosa of, 509 
cancer of, 511 
carcinoma of, 511 
circulatory disturbances of, 502 
colloid cancer of, 514 
congenital defects of, 502 
cylindrical cancer of, 514 
degeneration of mucous membrane of, 
508 

dilatation of, 509 
atonic, 509 

displacements of, 509 
fatty degeneration of cells of, 508 
hemorrhage of, 502 
hyperemia of, 502 
infectious diseases of, 510 
inflammation of, 521 

of mucosa of, 503 
malignant adenoma of, 514 
peptic ulcer of, 506 
pigmentation of mucosa of, 508 
polypoid elevations of, 510 
round ulcer of, 506 
softening of walls of, 509 
squamous cancer of, 514 
syphilitic gummata of, 510 
thrush of, 510 

tuberculous ulceration of, 510 
tumors of, 510 
Stomatitis, 484 
aphthous, 485 

associated conditions in, 487 
catarrhal, 484 
gangrenous, 486 
parasitic, 488 



868 



INDEX. 



Stomatitis, phlegmonous, 486 
pseudomembranous, 486 
ulcerative, 486 
Stone-particles, pigmentation by, 86 
Strangulated hernia, 517 
Strangulation, internal, of intestines, 
Stratified thrombi. 58 
Streptococci in kidney, 613 
Streptococcus, 190 

pyogenes seu erysipelatis, 212 
Streptococcus-toxin, 214 
Streptothrix, 190 
actinomyces, 258 
Madurae, 261 
Stricture of urethra, 634 

syphilitic, 532 
Strongylus longevaginatus, 308 
Struma, 576. See Goiter. 
aberrata suprarenalis, 609 
adenomatosa, 577 
Strumitis, acute, 576 
suppurative, 576 
Submucous abscess of intestine, 522 

fibroids, 650 
Subperitoneal fibroids, 650 
Substantia nigra. 745 
Substantial emphysema of lungs, 436 
Suffocation, 23 
Suffusion, definition of, 53 
Sugar in blood, 39 

in urine, 39 
Suggillation, definition of, 53 
Sulphate of copper, poisoning by. 25 
Sulphates in urine, 631 
Sulphuric acid, excessive formation 
in body. 36 
poisoning by, 25 
Supernumerary ovaries, 656 
Suprarenal bodies, 582 
accessory, 582 
adenoma of. 584 
amyloid degeneration of, 583 
carcinoma of, 584 
congenital abnormalities of, 582 
fatty degeneration of, 582 
general effects of diseases of. 584 
glioma of. 584 
hemorrhage from, 5S3 
inflammation of, 584 
neuroma of, 584 
pigmentation of, 583 
sarcoma of, 584 
syphilis of, 583 
tuberculosis of, 583 
tumors of, 584 
Suppurative bacterial diseases, 210 
cholangitis, 559 
encephalitis, 778 
enteritis, 522 
inflammation, 109 
lymphadenitis, 350 
myositis, 726 

chronic, 726 
nephritis, 592 
neuritis, 833 
pachymeningitis, 732 
pyelonephritis, 592 



Sympathetic nervous system, develop- 
ment of. 744 
Syncytioma malignum, 182 
Syncytium, 183, 673 
i Synovitis pannosa, 720 
517 Syphilis, 266 

congeuital, 270 
of arachnoid and pia, 740 
of arteries, 404 
of brain, 765 
of bone, 715 
of brain, 791 
of bronchi, 429 
of dura mater, 732 

of cord, 799 
of esophagus, 501 
of Fallopian tubes, 667 
of heart, 391 
of intestines, 532 
of joints, 723 
of kidney, 608 
of larynx, 422 
of liver, 552 
of lungs, 470 
of lymphatic glands, 355 

vessels, 416 
of mammary gland, 696 
of mouth, 489 
of muscles, 730 
of nasal cavities, 419 
of nerves, 833 
j of pancreas. 566 

of pericardium, 396 
i of pharynx, 497 
of, of pia and arachnoid of cord, 801 
of pituitary body, 796 
of placenta, 675 
of pleura, 482 
of spleen, 348 
of suprarenal bodies, 583 
of testicle, 686 
of thymus gland, 359 
of thyroid gland, 579 
of tongue, 489 
of trachea, 425 
of urethra, 636 
of uterus. 649 
of vagina, 672 
of vulva, 678 
secondary lesions of, 267 
tertiary lesions of. 267 
Syphilitic bubo. 267 

gummata of stomach, 510 
periostitis. 715 
pneumonia, congenital, 456 
stricture, 532 
Syphilomata, 268 
Syringomyelia, 805 

Tabes dorsalis, 817 
mesenterica, 355 
Tsenia Algeriana. 296 
cucumerina. 296 
echinococcus, 297 
elliptica, 296 
flavopunctata, 296 
Madagascarieusis, 296 



INDEX. 



809 



Taenia nana, 292, 295 

saginata, 294 

solium, 292 

tenella, 296 
Tape-worms, 290 

dwarf, 295 
Teeth, affections of, 490 
Temperature, high, effect of, 20 
Tendon-sheaths, inflammation of, 724 
Tenosynovitis, 724 

gonorrheal, 634 
Teratoma, 186 

of pia and arachnoid, 742 
Tertian fever, parasite of, 282 
Testicles, 681 

adenoma of, 687 ♦ 

adenosarcoma of, 687 

atheromatous cyst of, 689 

atrophy of, 681 

benign fungus of, 683 

calcification of, 682 

carcinoma of, 687 

caseation of, 682 

chondrocarcinoma of, 688 

chondroma of, 687 

congenital abnormalities of, 681 

cysts of, 688 

dermoid cysts of, 689 

echinococcus cysts of, 689 

fatty degeneration of, 682 

fibroma of, 687 

hyperemia of, 682 

hypertrophy of, 682 

inflammation of, 682. See Orchitis. 

lepra of, 687 

myxoma of, 687 

myxomatous degeneration of, 682 

osteoma of, 687 

papuliferous cystoma of, 688 

rhabdomyoma of, 687 

sarcoma of, 687 

syphilis of, 686 

syphilitic fungus of, 687 

tuberculosis of, 685 

tumors of, 687 
Tetanin, 258 
Tetanotoxin, 258 
Tetanus, 256 

antitoxin of, 258 

bacillus of, 256 
Texas fever of cattle, 285 
Thalamencephalon, 243 
Thermophilic bacteria, 196 
Thiothrix, 190 

Third ventricle of brain, 245 
Thoracic duct, diseases of, 417 
Thrombi, ball, 59 

calcification of, 60 

canalization of, 61 

degeneration of, 60 

marantic, 57 

organization of, 61 

purulent softening of, 60 

simple softening of, 60 

stratified, 58 
Thrombo-arteritis, 400 
Thrombophlebitis, 412 



Thrombosis, 57 
fermentation-, 58 
of bone, 706 
of brain, 773 
of cavities of heart, 364 
of coronary artery, 365 
of intestines, 520 
of kidney, 588 
of liver, 540 
of muscles, 725 
of spleen, 343 
of thoracic duct, 417 
| Thrombus, lateral, 59 
obstructive, 59 
primary, 59 
secondary, 59 
Thrush, 265, 488 
of esophagus, 501 
of stomach, 510 
Thymus gland, diseases of, 359 
Thyroid disease, general results of, 580 
gland, 575 

abscess of, 576 
actinomycosis of, 579 
adenoma of, 580 
anatomic considerations, 575 
carcinoma of, 580 
circulatory disturbances in, 576 
congenital defects of, 576 
general results of disease of, 580 
hyperemia of, 576 
inflammation of, 576 
sarcoma of, 580 
syphilis of, 579 
tuberculosis of, 579 
tumors of, 580 
Tissue-changes, progressive, 120 
Tissue-destruction, excessive, 34 
Tissue-elasticity, decreased, a cause of 
edema, 62 

Tissues, post-mortem degeneration of, 
101 

Toadstools, poisoning by, 29 
Tongue, actinomycosis of, 489 
furring of, 485 
geographical, 485 
nigrities of, 488 
syphilis of, 489 
tuberculosis of, 488 
Tonsil, abscess of, 495 
hypertrophy of, 495 
Tonsillitis, 494 
catarrhal, 494 
follicular, 494 
lacunar, 94 

phlegmonous, 494, 495 
Tophi of gout, 38 
Toxalbumins, 201 

from plants, poisoning by, 28 
Toxic products of bacteria, action of, 28 

effects of, 203 
Toxin of diphtheria, 223 
Toxin-immunity, 207 
Toxins, 201 
Toxophylaxins, 209 
Toxosozins, 209 
Trachea, 424 



870 



INDEX. 



Trachea, circulator}' disturbances of, 424 

inflammations of, 424 

malformations of, 424 

syphilis of, 425 

tuberculosis of, 425 

tumors of, 425 
Traction-diverticula of esophagus, 500 
Transitional leukocytes, 313 
Traumatic hemorrhage, 52 

theory of cause of carcinoma, 171 
Traumatism in etiology of disease, 19 
Trematodes, 308 
Trichina spiralis, 302 

in larynx, 424 
Trichiniasis, 303 
Trichobacteria, 192 
Trichocephalus dispar, 304 
Trichomonas caudata, 280 

el on gat a, 280 

flagellata. 280 

intestinalis, 280 

vaginalis, 280 
Trilocular heart, 361 
True hypertrophy, 121 

neuroma, 161 
Tubal abortion, 669 

pregnancy, 668 
Tube-cast in nephritis, 599 
Tubercle-bacillus, 233 

lymphoid, 239 

miliary, 237 

structure and evolution of, 238 

toxic properties of, 243 
Tubercula dolorosa, 162 
Tubercular leprosy, 246 

pneumonia, 219 
Tuberculin of Koch, 244 
Tuberculosis, 233 

acute pneumonic, 462 

avian, 245 

bacillus of, 233 

bronchogenic, 460 

chronic pneumonic, 463 

fowl-, 245 

gallinarum, 215 

hematogenic, 467 

latent, 243 

lymphogenic, 469 

miliary, 242 

of arteries, 404 

of bladder, 620 

of bone, 712 

of brain, 784 

of bronchi, 429 

of choroid plexus, 789 

of dura mater, 732 
of cord, 799 

of epididymis, 685 

of esophagus, 501 

of Fallopian tubes, 666 

of heart, 391 

of intestine, 531 

of joints, 722 

of kidney, 608 

of larynx, 422 

of liver, 551 

of lungs, 459 



Tuberculosis of lungs, bronchogenic, 459, 
460 

of lymphatic glands, 352 

of lymphatics, 416 

of mammary gland, 696 

of mouth, 588 

of muscle, 730 

of nasal cavities, 419 

of nerves, 833 

of ovary, 657 

of pancreas, 566 

of pelvis of kidnev, 615 

of penis, 680 

of pericardium, 396 

of peritoneum, 573 

of pharynx, 497 

of pia and arachnoid of cord, 801 

of pituitary body, 796 

of placenta, 675 

of pleura, 481 

of prostate, 690 

of seminal vesicles, 694 

of spleen, 347 

of suprarenal bodies, 583 

of testicle, 685 

of thoracic duct, 417 

of thymus gland, 359 

of thyroid gland, 579 

of tongue, 488 

of trachea, 425 

of urethra, 636 

of uterus, 648 

of vagina, 672 

of vas deferens, 686 

of veins. 415 

of vulva, 678 

pneumonic, 461 

relations of human, to animal, 236 

seats of, 242 
Tuberculous meningitis, 738 

pneumonia, 451 

ulceration of stomach, 510 
Tubo-ovarian cysts, 668 
Tubular adenoma, 167 
Tumor-dyscrasia, 171 
Tumors, 121 

benign, 126 

circumscribed, 125 

classification, 126 

dendritic, 125 

fungiform. 125 

fungoid, 125 

infiltrating, 125 

malignant, 126 

mixed, 136 

of arachnoid and pia, 740 

of biliary ducts, 561 

of bladder, 622 

of bone, 716 

of brain, 796 

of bronchi, 429 

of choroid plexus, 790 

of dura mater, 733 

of cord, 799 
of esophagus, 501 
of Fallopian tubes, 667 
of gall-bladder, 561 



INDEX. 



871 



Tumors of heart, 391 

of intestine, 533 

of joints, 723 

of kidney, 608 

of larynx, 423 

of liver, 553 

of lungs, 473 

of lymphatic glands, 355 
vessels, 416 

of mammary gland, 697 

of mouth, 490 

of muscles, 730 

of nasal cavities, 419 

of nerves, 834 

of ovaries, 658 

of pancreas, 566 

of pelvis of kidney, 616 

of penis, 680 

of pericardium, 396 

of peritoneum, 574 

of pharynx, 497 

of pituitary body, 796 

of pleura, 482 

of salivary glands, 498 

of seminal vesicles, 694 

of spinal cord, 827 

of spleen, 346 

of stomach, 510 

of suprarenal bodies, 584 

of teeth, 491 

of testicle, 687 

of thoracic duct, 417 

of thymus gland, 359 

of thyroid gland, 580 

of trachea, 425 

of ureter, 616 

of urethra, 636 

of uterus, 650 

of vagina, 672 
Tumors of veins, 414 

of vulva, 678 

papillary, 125 

polypoid, 125 

verrucose, 125 
Typhlitis, 523 

stercoral, 523 
Typhoid fever, 224, 528 
bacillus of, 224 
complications of, 530 
ulceration in, 501 
Typhus fever, bacteriology of, 274 

icteroides, 271 

recurrens, 262 
Tyroma, meningeal, 739 
Tyrosin in urine, 36, 631 
Tyrotoxicon, 30 

Ulcer, 111 

indolent, 111 

peptic, of intestines, 522 

phagedenic, 111 

serpiginous, 111 
Ulceration of intestines, 522 

typhoid, 501 
Ulcerative dysentery, 527 

endocarditis, 368 

esophagitis, 500 



Ulcerative gastritis, 503 

stomatitis, 486 
Ulcers of bronchi, 428 
Ulcus ex digestione, 506 
Umbilical cord, abnormalities of, 673 

velamentous insertion of, 673 
Urate of sodium deposit in tissues, 86 
Urates in urine, 630 
Uratic infiltration, 86 
Urea, formation of, 35 
Uremia from nephritis, 603 
Ureter, 613 

dilatation of, 613 

inflammation of, 615 

malformations of, 613 

obstructions of, 613 

parasites of, 616 

tumors of, 616 
Ureteritis, 615 
Urethra, 632 

carcinoma of, 636 

congenital abnormalities of, 632 

cysts of, 636 

inflammation of, 632 

injuries of, 635 

sarcoma of, 636 

stricture of, 634 

tuberculosis of, 636 

tumors of, 636 
Urethritis, 632 

anterior, 633 

associated lesions of, 633 

posterior, 634 
Uric acid calculi, 621 

crystals in urine. 629 
excretion of, in gout, 38 
formation of, 37 
Urinarv bladder. See Bladder. 

calculi, 621 
results of, 622 

organs, congenital anomalies of, 585 
Urine, abnormal conditions of, 624 

bacteria in, 628 

bilirubin in, 631 

carbonates in, 631 

chemic changes in, 629 

cholesterin in, 631 

color of, 624 

cystin in, 631 

fat-crystals in, 631 

hippuric acid in, 630 

indigo in. 631 

in nephritis, 599 

leucin in, 631 

oxalate of urine in, 629 

phosphates in, 629 

quantity of, 624 

reaction of, 624 

sediments of, 629 

specific gravity of, 624 

sulphates in, 631 

tyrosin in, 631 

urates in, 630 

uric acid crystals in, 629 

xanthin in, 631 
Uriniferous tubules, concretions in, 607 
Urobilin uria, 625 



872 



INDEX. 



Uschinsky's fluid, 197 
Uterus, 636 

adenoma of, 652 
malignant, 652 

amyloid degeneration of, 649 

anteflexion of, 638 

anteversion of, 638 

bicornis, 637 

carcinoma of, 652 

congenital abnormalities, 637 

cysts of, 655 

dilatation of, 640 

erosions of, 645 

fattv degeneration of, 649 

fibroid of, 650 
polyps of, 650 

fcetalis seu infantilis. 637 

hemorrhages of, 642 

hyperemia of, 641 

hyperplasia of mucous membrane of, 649 

hypertrophy of, 649 

hypoplasia of, 637 

inflammation of, 642 

inversion of, 640 

lateral displacements of 638 

leiomyoma of, 650 

myofibroma of, 650 

parasites of, 655 

polyps of, 650 

prolapse of, 638 

puerperal atrophy of, 649 

infections of, 646 
retroflexion, 638 
rupture of, 641 
sarcoma of, 652 
senile atrophy of, 649 
septus, 637 
stenosis of, 640 
syphilis of, 649 
tuberculosis of, 648 
tumors of, 650 
unicornis, 638 
upward dislocation of, 638 

Vaccinia, animal parasites of, 290 
Vacuolation of red blood-corpuscle, 319 
Vacuolization of nerve-cell, 756 
Vagina, 670 

carcinoma of, 672 

circulatory disturbances of, 671 

cysts of, 672 

fibroma of, 672 

hyperemia of, 671 

inflammation of, 671. See Vaginitis. 

myofibroma of, 672 

papilloma of, 672 

sarcoma of, 672 

stenosis of, 670 

syphilis of, 672 

tuberculosis of, 672 

tumors of, 672 
Vaginal cystocele, 670 

rectocele, 670 

wall, prolapse of, 670 

wounds and fistulse of, 670 
Vaginitis, 671 

acute catarrhal, 671 



Vaginitis, chronic catarrhal, 671 
exfoliative, 671 
pseudomembranous, 671 
testis, 682, 684 
hemorrhagic, 685 
purulent, 685 
serofibrinous, 684 
serous, 684 
Valvular defects, 362 
Varicella, micro-organism of, 290 
Varicose aneurysm, 411 

veins of spinal cord, 810 
Varicosity, 413 

Variola, animal parasites of, 290 
Vas deferens, inflammation of, 685 

tuberculosis of, 686 
Vascular goiter, 578 

theories of inflammation, 101 
Vein-stones, 412 
Veins, 411 

calcification of, 412 

dilatation of, 413 

fatty degeneration of, 412 

inflammation of, 412 

tuberculosis of, 415 

tumors of, 414 
Venereal wart, 164 
Venom of serpents, poisoning by, 28- 
Venous hemorrhage, 50 

hyperemia, 48 
Ventricular septum, defects of, 362 
Verrucose endocarditis, 368 

tumors, 125 
Vesica bipartitis, 617 
Vesicular emphysema of lungs, 436> 
Vibrio cholera? Asiatic®, 229 
Vibrion septique, 251 
Vicarious emphysema of lungs, 436 
Virchow's theory of inflammation. 101 

classification of tumors, 127 

theory of tumors, 123 
Voluntary muscles, diseases of, 724 
Volvulus, 518 
Vulva, 677 

abscess of, 677 

adenoma of, 678 

carcinoma of, 679 

chancroids of, 678 

circulatory disturbances of, 677 

cysts of, 679 

diphtheria of, 678 

elephantiasis of, 678 

fibroma of, 678 

fibromyxoma of, 678 

gangrene of, 678 

hematoma of, 677 

hyperemia of, 677 

inflammation of, 677 

lipoma of, 678 

myofibroma of, 678 

papillomatous tumors of, 678 

sarcoma of, 678 

syphilis of, 678 

tuberculosis of, 678 

tumors of, 678 

wounds of, 677 
Vulvitis, 677 



INDEX. 



873 



Wart, 164 

veuereal, 164 
Waxy casts in nephritis, 600 
Wens, 184 

White blood-corpuscles, 312. See Leuko- 
cytes. 
infarct, 56 

matter of cord, degeneration of, 824 

softening of brain, 774 
Whooping-cough, bacteriology of, 273 
Widal reaction, 227 
Wool-sorters' disease, 252 
Wounds, repair of, 112 



Xanthin, 37 

in urine, 631 
Xanthoma, 133 

diabeticorum, 133 

vulgare, 133 

Yellow fever, 271 
antitoxin of, 272 
bacillus of, 272 
softening of brain, 774 

Ziehl's solution, 194 
Zuckergussleber, 551, 573 



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